– If you have both diabetes and high cholesterol, you’re not alone. The American Heart Association (AHA) states that diabetes often lowers HDL (good) cholesterol levels and raises triglycerides and LDL (bad) cholesterol levels. Both of these increase the risk for heart disease and stroke. As a reminder:
An LDL cholesterol level under 100 milligrams/deciliter (mg/dL) is considered ideal.100–129 mg/dL is close to ideal.130–159 mg/dL is borderline elevated.
High cholesterol levels can be dangerous. Cholesterol is a type of fat that can build up inside the arteries. Over time, it can harden to form a stiff plaque. That damages arteries, making them stiff and narrow and inhibiting blood flow. The heart has to work harder to pump blood, and risk for heart attack and stroke go up.
- Researchers don’t have all the answers yet and continue to grapple with how diabetes and high cholesterol are related.
- In one study published in The Journal of Lipid Research, they found that blood sugar, insulin, and cholesterol all interact with each other in the body, and are affected by each other.
They just weren’t sure exactly how. Meanwhile, what’s important is that you’re aware of the combination between the two. Even if you keep your blood sugar levels under control, your LDL cholesterol levels may still go up. However, you can control both of these conditions with medications and good lifestyle habits.
Why does diabetes cause high lipids?
Conclusions – Abnormalities of lipoprotein metabolism are one of the major factors contributing to cardiovascular risk in patients with type 2 diabetes, and diabetic dyslipidaemia includes not only quantitative but also qualitative and kinetic lipoprotein abnormalities that are inherently atherogenic.
The primary (characteristic) quantitative abnormalities are hypertriglyceridaemia, accompanied by prolonged postprandial hyperlipidaemia and increased levels of remnant particles (related to the increased production of triacylglycerol-rich lipoproteins and a reduction in the rate of catabolism of triacylglycerol-rich lipoproteins), and decreased HDL-cholesterol levels secondary to an increased rate of HDL catabolism.
The most frequent qualitative abnormalities, which are potentially atherogenic, include an increase in large VLDL particle size (VLDL 1 ); a greater proportion of small, dense LDL particles; an augmented susceptibility of LDLs to oxidation; an increase in triacylglycerol content of both LDL and HDL; and glycation of apolipoproteins.
- Although levels of LDL may be normal in patients with type 2 diabetes, LDL plasma residence time is increased due to a slower turnover rate, and this may infer the promotion of lipid deposition within artery walls.
- Furthermore, the usual cardioprotective effects of HDL are reduced or abolished in type 2 diabetes.
Some factors, such as insulin resistance and possibly some adipokines (e.g. adiponectin) and hyperglycaemia, are involved in the pathophysiology of diabetic dyslipidaemia. However, many questions remain unanswered (such as the pathophysiology and the consequences of the qualitative lipid abnormalities, the precise mechanisms and signalling pathways involved in the insulin resistance linked lipid abnormalities, the potential role of adipose tissue and adipocytokines in the pathophysiology of diabetic dyslipidaemia) and additional studies are needed to gain further insight into the precise mechanisms of diabetic dyslipidaemia.
What is the effect of diabetes on blood lipids?
Table 1 – Characteristics of the study participants by the level of glucose intolerance.
| Variable | Normal (n = 1915) | Prediabetes (n = 197) | T2DM (n = 181) | p for Trend |
|---|---|---|---|---|
| Age (years) | 41.2 (40.6, 41.8) | 44.2 (42.3, 46.1) * | 45.8 (43.8, 47.7) * | <0.001 |
| Female, % | 64.6 (49.9, 63.8) | 56.9 (50.0, 63.8) | 55.8 (48.5, 63.1) | 0.003 |
| Body Mass Index (kg/m 2 ) | 22.3 (22.2, 22.5) | 24.3 (23.7, 24.8) * | 24.4 (23.8, 24.9) * | <0.001 |
| BMI (≥25 kg/m 2 ), % | 23.1 (21.2, 24.9) | 43.2 (36.3, 50.1)* | 41.4 (34.2, 48.6) * | <0.001 |
| Waist (cm) | 79.4 (78.9, 79.9) | 84.8 (83.3, 86.4) * | 86.9 (85.5, 88.3) * | <0.001 |
| Waist: M ≥ 90 & F ≥ 80 cm, % | 36.1 (33.9, 38.1) | 56.4 (49.7, 63.0) * | 62.1 (55.4, 68.9) *,† | <0.001 |
| SBP (mmHg) | 115.3 (114.6, 116.0) | 118.3 (116.6, 120.0) * | 120.9 (1191, 122.6) *,† | <0.001 |
| DBP (mmHg) | 76.6 (76.1, 77.0) | 78.0 (77.0, 79.1) * | 79.4 (78.3, 80.5) * | <0.001 |
| Hypertension, % | 14.4 (12.8, 15.9) | 17.0 (12.0, 21.9) | 24.8 (18.9, 30.7) *,† | <0.001 |
| FPG (mmol/L) | 4.7 (4.6, 4.8) | 5.7 (5.5, 5.9) * | 9.5 (9.3, 9.7) *,† | <0.001 |
| 2hPG (mmol/L) | 5.4 (5.3, 5.5) | 7.5 (7.4, 7.9) * | 13.9 (13.8, 14.2) *,† | <0.001 |
| Fasting insulin (µIu/mL) ± | 7.9 (7.8, 8.2) | 10.5 (9.4, 11.6) * | 11.5 (10.5, 12.5) * | <0.001 |
| HOMA-IR ± | 1.50 (1.45, 1.54) | 2.36 (2.12, 2.64) * | 4.14 (3.67, 4.71) *,† | <0.001 |
| T-Chol (mmol/L) | 4.3 (4.2, 4.4) | 4.5 (4.4, 4.6) * | 4.9 (4.7, 5.0) *,† | <0.001 |
| T-Chol ≥ 5.2 mmol/L, % | 8.7 (7.5, 10.0) | 13.2 (9.1, 18.7) * | 26.0 (20.1, 32.9) *,† | <0.001 |
| Tg (mmol/L) ± | 1.3 (1.1, 1.4) | 1.5 (1.3, 1.6) * | 1.9 (1.8, 2.1) *,† | <0.001 |
| Tg ≥ 1.7 mmol/L, % | 26.1 (24.2, 28.1) | 42.1 (35.4, 49.2) * | 63.5 (56.3, 70.2) *,† | <0.001 |
| HDL-C (mmol/L) | 0.91 (0.90, 0.92) | 0.86 (0.82, 0.89) * | 0.81 (0.77, 0.85) *,† | <0.001 |
| HDL-C: M:<1.04 & F:<1.3 mmol/L, % | 91.3 (90.0, 92.5) | 97.0 (93.4, 99.0) * | 95.6 (91.4, 97.8) * | 0.004 |
| LDL-C (mmol/L) | 2.76 (2.72, 2.78) | 2.80 (2.70, 2.89) | 2.84 (2.75, 2.92) | 0.016 |
| LDL-C ≥ 3.4 mmol/L, % | 11.3 (9.9, 12.8) | 16.2 (11.7, 22.1) * | 16.0 (11.4, 22.1) | 0.014 |
| High Tg & Low HDL-C, % | 24.6 (22.7, 26.6) | 40.0 (33.2, 46.7) * | 58.7 (51.5, 65.9) *,† | <0.001 |
Adjusted means of FPG, 2hPG, fasting insulin, HOMA-IR, T-Chol, Tg, and HDL-C levels varied significantly between the different stages of glucose intolerance ( Table 1 ). Except for the HDL-C which was negatively associated with the level of glucose intolerance, positive linear trends were observed ( p -value for trend 90%) in all groups of glucose intolerance. The prevalence of high Tg varied from 26.1% in those with NGT to 63.5% in those with T2DM ( Table 1 ). The proportions having high T-Chol, high Tg, low HDL-C, combined high Tg and low HDL-C were significantly higher among participants with T2DM and prediabetes than those with NGT. In participants with NGT, 24.5% had high Tg combined with low HDL-C, whereas the corresponding prevalence in those with T2DM was 58.7%. The proportion of participants with T2DM and prediabetes by different lipid parameters are displayed in Figure 1, The proportion of T2DM among those with normal or high T-Chol; normal or high Tg; normal or high LDL-C; and normal or low HDL-C groups were: 6.6 vs.18.4% ( p < 0.001); 4.2 vs.16.1% ( p < 0.001); 7.6 vs.10.0% ( p = 0.162); and 4.1 vs.8.2% ( p = 0.048), respectively. Prevalence of prediabetes and T2DM by different lipid parameters. The proportion of prediabetes among those with normal or high T-Chol; normal or high Tg; normal or high LDL-C; and normal or low HDL-C groups were: 8.3 vs.10.4% ( p = 0.280); 7.2 vs.11.7% ( p = 0.001); 8.1 vs.11.2% ( p = 0.091); and 3.2 vs.9.1% ( p = 0.009), respectively. No significant differences were observed in the proportion of T2DM and prediabetes between high or normal LDL-C groups. Data are presented as percentages (95% confidence interval) adjusted for age. Independent variables were categorized as follows: T-Chol (normal < 5.2 vs. high ≥ 5.2 mmol/L); Tg (normal < 1.7 vs. high ≥ 1.7 mmol/L); HDL-C (normal M ≥ 1.04 and F ≥ 1.3 vs. Low M <1.04 and F < 1.3 mmol/L); LDL-C (normal < 3.4 vs. high ≥ 3.4 mmol/L). Abbreviation: T2DM, type 2 diabetes mellitus; T-Chol, total cholesterol; Tg, triglycerides; LDL-C, low density lipoprotein cholesterol; HDL-C, high density lipoprotein cholesterol. Table 2 shows the odds ratio (OR) of different lipid parameters for the risk of having T2DM and prediabetes. T2DM showed a significant association with T-Chol (OR): 2.43, p < 0.001); Tg (OR: 3.91, p < 0.001); and HDL-C (OR: 2.17, p = 0.044). Prediabetes showed a significant association with Tg (OR: 1.96, p < 0.001) and HDL-C (OR: 2.93, p = 0.011).
How does diabetes affect cholesterol levels?
Cholesterol and diabetes Diabetes damages the lining of your arteries. This means it’s more likely that cholesterol will stick to them, making them narrow or even blocked. If you have diabetes, you will usually have lower levels of HDL (good) cholesterol and higher levels of LDL/non-HDL (bad) cholesterol.
Are lipids related to diabetes?
Skip Nav Destination Article navigation Reviews/Commentaries/Position Statements | June 01 2004 Ronald M. Krauss, MD From the Children’s Hospital Oakland Research Institute, Oakland, California Search for other works by this author on: Address correspondence and reprint requests to Ronald M. Krauss, MD, 5700 Martin Luther King Jr. Way, Oakland, CA 94609. E-mail: [email protected] Diabetes Care 2004;27(6):1496–1504 Insulin resistance and type 2 diabetes are associated with a clustering of interrelated plasma lipid and lipoprotein abnormalities, which include reduced HDL cholesterol, a predominance of small dense LDL particles, and elevated triglyceride levels.
Each of these dyslipidemic features is associated with an increased risk of cardiovascular disease. Increased hepatic secretion of large triglyceride-rich VLDL and impaired clearance of VLDL appears to be of central importance in the pathophysiology of this dyslipidemia. Small dense LDL particles arise from the intravascular processing of specific larger VLDL precursors.
Typically, reduced plasma HDL levels in type 2 diabetes are manifest as reductions in the HDL 2b subspecies and relative or absolute increases in smaller denser HDL 3b and HDL 3c, Although behavioral interventions such as diet and exercise can improve diabetic dyslipidemia, for most patients, pharmacological therapy is needed to reach treatment goals.
- There are several classes of medications that can be used to treat lipid and lipoprotein abnormalities associated with insulin resistance and type 2 diabetes, including statins, fibrates, niacin, and thiazolidinediones.
- Clinical trials have shown significant improvement in coronary artery disease after diabetic dyslipidemia treatment.
Type 2 diabetes is associated with a cluster of interrelated plasma lipid and lipoprotein abnormalities, including reduced HDL cholesterol, a predominance of small dense LDL particles, and elevated triglycerides (1). These abnormalities occur in many patients despite normal LDL cholesterol levels.
These changes are also a feature of the insulin resistance syndrome (also known as the metabolic syndrome), which underlies many cases of type 2 diabetes. In fact, pre-diabetic individuals often exhibit an atherogenic pattern of risk factors that includes higher levels of total cholesterol, LDL cholesterol, and triglycerides and lower levels of HDL cholesterol than individuals who do not develop diabetes (2,3).
Insulin resistance has striking effects on lipoprotein size and subclass particle concentrations for VLDL, LDL, and HDL (4,5). There is evidence that each of these dyslipidemic features is associated with increased risk of cardiovascular disease, the leading cause of death in patients with type 2 diabetes.
- Numerous studies have demonstrated an association between LDL size or density and coronary artery disease (CAD) (6–13).
- Moreover, recent reports have indicated that LDL particle concentrations, and specifically levels of small dense LDL, are predictive of coronary events and that this is independent of other coronary disease risk factors (14–16).
Although lowering LDL cholesterol is important in decreasing cardiovascular disease morbidity and mortality, there are a number of other factors contributing to the disease process that can be favorably affected by drug therapy. Among these factors are subspecies of the major lipoprotein classes, such as triglyceride-rich lipoprotein remnants and small dense LDL, that are not detected by standard lipid testing.
- It is therefore possible that at least part of the CAD benefits observed in CAD prevention trials can be attributed to pharmacological effects on specific types of lipoprotein particles.
- This article will review the pathophysiology of diabetic dyslipidemia and the relationship between reduced HDL levels, increased small dense LDL particles, elevated triglycerides, and cardiovascular risk.
Current therapeutic options for the management of diabetic dyslipidemia and clinical trials that provide evidence of the benefits of treating this atherogenic dyslipidemia also will be discussed.
How does type 2 diabetes affect lipid metabolism?
Abstract – Diabetes mellitus is the most frequent endogenous cause of fat metabolism-disorder. In diabetics the risk for arteriosclerosis is significantly higher and the clinical significance of hyperlipidemia should be estimated more serious as in non-diabetics.
The predominant abnormality of fat metabolism in diabetes is hypertriglyceridemia due to an increase of triglyceride-carrying lipoproteins, the chylomicrons and the very-low-density lipoproteins. In type I-diabetics the decisive pathogenetic factor for hypertriglyceridemia is the impaired degradation of VLDL and the reduced chylomicron-clearance, caused by decreased activity of the lipoproteinlipase.
In ketoacidosis there is an additional increase in hepatic VLDL-triglyceride-production due to increased lipolysis with elevated free-fatty-acid flux. Total cholesterol in type I-diabetics is only significantly elevated when metabolic control is poor, low-density lipoprotein (LDL-)-cholesterol-levels can be increased and high-density lipoprotein (HDL-)cholesterol decreased in dependence on the metabolic control.
- In type II-diabetics the decisive pathogenetic factor for hypertriglyceridemia is increased VLDL-triglyceride-synthesis in the liver especially due to augmented free-fatty-acid flux.
- Additionally the activity of the lipoproteinlipase can be reduced.
- Usually in non-insulin-dependent diabetics LDL-cholesterol-levels can be seen elevated and HDL-cholesterol-concentration decreased in correlation with the metabolic control.
Primary hyperlipoproteinemia appears frequently in diabetics, but this can be explained by the association with obesity in type II-diabetics.
Why does diabetes increase triglycerides?
Recap – There are many causes of high triglycerides. If you have diabetes, the way that your body handles some foods (like carbohydrates and sugar) can contribute to high triglyceride levels. Other health conditions, medications, and genetics can also lead to triglyceride levels that are too high.
How is glucose and lipids related?
Glucose and lipid metabolism are linked to each other in many ways. The most important clinical manifestation of this interaction is diabetic dyslipidemia, characterized by elevated triglycerides, low high density lipoprotein cholesterol (HDL-C), and predominance of small-dense LDL particles.
How does insulin relate to lipids?
Insulin stimulates the uptake of glucose, amino acids and fatty acids into cells, and increases the expression or activity of enzymes that catalyse glycogen, lipid and protein synthesis, while inhibiting the activity or expression of those that catalyse degradation.
How does insulin affect lipid profile?
Abstract – The 3 major components of the dyslipidemia of insulin resistance are increased triglyceride levels, decreased high-density lipoprotein (HDL) cholesterol, and changes in the composition of low-density lipoprotein (LDL) cholesterol. Hyperinsulinemia and the central obesity that typically accompanies insulin resistance are thought to lead to overproduction of very low-density lipoprotein (VLDL) cholesterol.
The result is more triglyceride-rich particles, fewer HDL particles, and more small, dense LDL. Postprandial triglyceride levels and measures of postprandial remnants also may contribute to increased coronary artery disease (CAD) risk in individuals with insulin resistance. Deficiency of lipoprotein lipase, an insulin-sensitive enzyme, might explain the abnormal levels of remnant particles in insulin resistance.
The potential benefits of successful treatment of dyslipidemia are illustrated by clinical trials in patients with the dyslipidemia characteristic of insulin resistance (i.e., normal or only moderately elevated LDL, elevated VLDL, and low HDL). Both weight loss and exercise can improve insulin resistance and associated dyslipidemia.
Is high blood lipid levels a symptom of diabetes?
What’s the Connection? – Cholesterol is a waxy substance in your blood. Your body makes it. Cholesterol isn’t a bad substance. It helps make the outer layer of our cells and helps make certain vitamins and hormones. It’s also in meat, cheese, and other foods from animals. But too much cholesterol in your blood can lead to health issues. There are different types of cholesterol:
Low-density-lipoprotein ( LDL ) cholesterol, or “bad” cholesterol. When your LDL cholesterol levels are too high, your arteries can become too narrow and get blocked. This can cause stroke and heart problems. High-density-lipoprotein (HDL) cholesterol, or “good” cholesterol. Low levels of HDL cholesterol can contribute to heart disease and other issues, especially if your LDL cholesterol and triglyceride levels are high. Triglycerides, These are fats from the food you eat that circulate in your body, which can be stored in fat cells. Triglycerides aren’t actually a type of cholesterol, but their levels are measured along with HDL and LDL in order to determine your odds of developing atherosclerosis (which is when fatty deposits build up in your artery walls). Atherosclerosis puts you at risk for heart attacks, strokes, and peripheral artery disease,
If you have type 2 diabetes and have your blood sugar under control, you still might have high levels of triglycerides and low HDL levels. You may also have higher levels of LDL cholesterol, too. Having poor blood sugar control can make cholesterol levels worse.
- If you have diabetes and have low levels of good cholesterol but high levels of bad cholesterol and high triglycerides, you have a condition called diabetic dyslipidemia.
- Up to 70% of people with type 2 diabetes have diabetic dyslipidemia.
- One reason diabetes is linked with heart disease is because people with diabetes tend to have LDL particles that are smaller and denser than those who don’t.
This gives it more of a chance to invade blood vessel walls and create plaque in your arteries. People with type 1 diabetes who have their blood sugar under control usually have normal levels of cholesterol. If they’re overweight or have obesity, though, they’re more likely to have high cholesterol.
Does insulin increase lipids?
Insulin and Lipid Metabolism – The metabolic pathways for utilization of fats and carbohydrates are deeply and intricately intertwined. Considering insulin’s profound effects on carbohydrate metabolism, it stands to reason that insulin also has important effects on lipid metabolism, including the following: 1. Insulin promotes synthesis of fatty acids in the liver. As discussed above, insulin is stimulatory to synthesis of glycogen in the liver. However, as glycogen accumulates to high levels (roughly 5% of liver mass), further synthesis is strongly suppressed.
When the liver is saturated with glycogen, any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which are exported from the liver as lipoproteins. The lipoproteins are ripped apart in the circulation, providing free fatty acids for use in other tissues, including adipocytes, which use them to synthesize triglyceride.2.
Insulin inhibits breakdown of fat in adipose tissue by inhibiting the intracellular lipase that hydrolyzes triglycerides to release fatty acids. Insulin facilitates entry of glucose into adipocytes, and within those cells, glucose can be used to synthesize glycerol.
Why does HDL decrease in diabetes?
INTRODUCTION – Many patients with type 2 diabetes have a low concentration of high density lipoprotein cholesterol (HDL-C). The fact that a low level of HDL-C is a predictor of cardiovascular disease, it follows that a low level of HDL-C in patients with type 2 diabetes may contribute to the increased cardiovascular risk associated with this condition.
- The precise cause of the low HDL-C in type 2 diabetes is not known but may be the consequence of insulin resistance, augmented very low density lipoprotein production and increased activities of cholesteryl ester transfer protein (CETP) and endothelial lipase.
- Recent studies showing that HDLs have the ability to improve increase the uptake of glucose by skeletal muscle and to stimulate the secretion of insulin from pancreatic beta cells raise the possibility that the low HDL concentration in type 2 diabetes may also contribute to a worsening of diabetic control or, indeed, to the progression of prediabetes to the full diabetic state.
Therefore, a low concentration of HDLs may not only be a consequence of the diabetes and a contributor to the increased cardiovascular risk in diabetics but may also result in a worsening of glycemic control in people with type 2 diabetes.
Are high triglycerides related to diabetes?
Background – Although there is abundant evidence indicating the connection between triglyceride and type 2 diabetes mellitus (T2DM), few reports or cohort studies confirm that high TG concentration may predict the incidence of T2DM independently. Thus, we studied the association between triglyceride (TG) and T2DM in a male-dominated, middle and older aged cohort, Tianjin General Hospital Cohort.
How does sugar affect cholesterol and triglycerides?
By Spencer Kroll, MD, PhD It is a well-known fact that the war is on against sugar. Many people don’t realize that sugar and other carbohydrate consumption can also contribute to cholesterol problems. In fact, sugar ─ in the form of table sugar (sucrose) or high-fructose corn syrup ─ can be a greater contributor to heart disease than the consumption of saturated fat, long regarded as the main contributor to this condition.
Most Americans consume far too much sugar on a daily basis. Why? There are a multitude of reasons. For example, many of us are unaware that processed foods are loaded with hidden sugars to enhance flavor. In addition to all the fructose added, Americans consume an average of 22 teaspoons of sugar a day and even more from carbohydrates (which the body breaks down into sugar) from pasta, rice, bread, corn and potatoes.
For the last 30 years, our dietary focus has been to reduce fats in our diets. As a result, there has been an increase in carbohydrate consumption resulting in an epidemic of pre-diabetes and diabetes along with a new type of cholesterol problem. Cholesterol reduction requires a one-on-one treatment regime As a physician and lipidologist (a doctor specializing in cholesterol management), I work with people on an individual basis to help them lower their cholesterol based upon their unique lifestyle and personal healthcare needs.
- This is extremely important because “one size does not fit all” when it comes to managing cholesterol.
- Every patient’s blood work, medical history, age and overall health should be taken into account when determining the best treatments for lowering cardiovascular disease.
- Sugar consumption negatively affects “good and bad” cholesterol Standard cholesterol measurement reveals your total cholesterol level broken down by LDL (bad cholesterol), HDL (good cholesterol) and triglycerides.
LDL elevation, which is linked in part to saturated fat intake, is only one type of cholesterol problem. How is sugar a major culprit in cholesterol problems? Eating sugar and other carbohydrates raises triglycerides and lowers HDL. It also causes dysfunctional alterations in LDL molecules.
- LDL levels may seem normal, but this dysfunctional LDL can cause rapid clogging of arteries and increased risk for thrombosis.
- Reducing sugar intake offers big rewards Generally speaking, the goal for many people is to reduce daily sugar intake and realize that carbohydrates must also be reduced to impact your cholesterol problems.
Avoid high fructose corn syrup. The brain cannot sense this form of sugar like it does regular table sugar and this will cause you to eat more before feeling full. After about five days of living on fewer carbohydrates, my patients report feeling much more energy, less stress and even craving healthier food choices.
- So give your body a gift that will keep on giving.
- Dump the sugar and reduce the carbs.
- Your cholesterol, heart, mind and body will thank you for it.
- CentraState Medical Center in Freehold offers an extensive roster of board-certified physicians and medical specialists throughout the region.
- To find a family or internal medicine physician near you, call 866-CENTRA7 ( 866-236-8727 ), or visit the Physician Finder at centrastate.com/physicians.
In addition, CentraState’s Star and Barry Tobias Health Awareness Center (HAC) offers more than 200 health education and lifestyle management programs to help patients achieve their health and wellness goals. A dedicated team of registered nurses, registered dietitians, lifestyle management experts and integrative therapy practitioners help participants to lose weight, get fit, eat healthy and lower disease risk. Spencer Kroll, MD, PhD is a board-certified, Georgetown University-trained physician specializing in internal medicine and a board-certified lipidologists. He is also a fellow of the National Lipid Association. Dr. Kroll is on staff at CentraState Medical Center and may be reached at his Morganville office by calling (732) 591-8840,
Are triglycerides and blood sugar related?
A Study Measuring the Effect of High Serum Triglyceride and Cholesterol on Glucose Elevation in Human Serum The purpose of this study is to further confirm the results documented in previous studies and to test the hypothesis of the presence of any correlation and if found, the regression nature of such correlation between triglyceride and glucose levels in one hand and cholesterol and glucose levels in the other hand. Samples were collected between March and August 2009 from 438 of both males and females from two patient groups; a) non-diabetic patients, b) non-insulin dependent type II diabetic patients. The patients’ serum glucose; cholesterol and triglyceride were simultaneously determined. A comparison study was conducted on the effect of the elevated level of each of the parameters (Cholesterol and Triglyceride) on glucose elevation. The results showed that there was a significant difference in the number of cases with high glucose values >110 mg/dl among the three different study groups. There was a significant difference in the number of cases with glucose values >110 mg/dl between the two different study groups; 1) triglyceride 201 mg/dl, 2) triglyceride >151 mg/dl and cholesterol>201 mg/dl. The elevation in triglyceride but not cholesterol has the same effect of both triglyceride and cholesterol elevation together on the association with increasing levels of high glucose in blood. Keywords: Glucose, Cholesterol, Triglyceride, Association In previous studies measuring the effect of high serum triglyceride and cholesterol on glucose elevation in human serum, it was demonstrated that high serum triglyceride has a well-established association and impact on increasing cases of high glucose levels in blood, – while elevation in serum cholesterol alone has no real association or impact on increasing cases of high glucose levels in human blood. Most of the studies conducted on glucose have mentioned that 90-95% of the diabetic cases were type II diabetes mellitus. This adult type of diabetes affects older people who are obese or over weight, or have a family history of diabetes, and have restricted movement or limited exercise. In a primary study on 3000 human individuals who are in their preliminary stages of the diabetes symptoms, the results showed that decreasing weight between 5-7% on the study participants had preventive properties on 60% of the participants from developing real diabetes. Their weight was achieved by stopping the consumption of fats and by exercising. The studies on type II diabetes revealed that the patients have problems in lipids concentration and metabolism. It was concluded that decreasing serum Lipids and triglyceride concentration will decrease blood glucose in the human body. In a study monitoring lipid toxicity, the results revealed that hypertriglycemia is essential for lipid toxicity to develop. Lipid toxicity would not occur in the absence of blood glucose elevation. The study concluded that lipids and glucose toxicity are interrelated and that the effect of glucose on lipid metabolism is essential. Therefore, lipids toxicity is to be associated as manifestation of glucose toxicity. In another study evaluating sterol excretion and cholesterol absorption in diabetics and non-diabetics with /without hyperlipidemia, the results indicated that sterol excretion is elevated in those who are hyperlipidemic. It was further elevated in patients with both diabetes and hyperlipidemia. However, there was no significant difference in absorbed cholesterol and excretory sterol between diabetic or non-diabetic patients with the same serum triglyceride concentrations. The study also showed that the problem mostly associated with diabetes mellitus is hypertriglyceremia, which is associated with triglyceride and very low density lipoproteins (VLDL) synthesis but not decomposition. The study also indicated that there was no significant difference in synthesized and absorbed cholesterol between diabetic and non-diabetic patients involved in the study. The elevation in cholesterol syntheses in diabetics was due to the hyperlipidemia and more specifically due to hypertriglyceremia associated with triglyceride elevated in the serum. Thus, there was no direct association between cholesterol absorption, synthesis, excretion or blood glucose levels. While a study assessing lipid and carbohydrate metabolism in type II diabetic patients revealed that a diet-rich in glucose caused prolonged elevation in serum triglyceride. Furthermore, a study conducted to determine the “relationship of Obesity to Serum Triglyceride, Cholesterol, and Uric Acid, and to Plasma-Glucose Levels” indicated that blood hypercholesterolemia was associated with blood hypertriglyceremia, meaning that both cholesterol and triglyceride elevation are not independent of each other. Moreover, a preliminary observation conducted to assess the Genetic Association Between Insulin Resistance And Total Cholesterol In Type II Diabetes Mellitus in Sri Lanka, showed that 69% of type II diabetics had a significant elevation in cholesterol. While another in Nigeria based on exercise performance in relation to glucose drink and their effect on some biochemical parameters, the study highlighted significant elevations in blood glucose and serum triglyceride after 30-60-150 minutes of glucose rich drink consumption and jogging. This study was conducted to further confirm the results documented in previous studies and to test the hypothesis of the presence of any correlation and if found, the regression nature of such correlation between triglyceride and glucose levels in one hand and cholesterol and glucose levels in the other hand. Samples were collected from patients who came to the Daboul Medical laboratory, Damascus city, Syria, between March and August 2009. The samples were gathered from two patient types; a) non-diabetic patients who came for general laboratory check-up, and b) non-insulin dependent type II diabetic patients. The study group consisted of 438 patients of both males and females aged between 38-86 years who had their blood drawn and fasting serum glucose, cholesterol and triglyceride were simultaneously determined. The patients were divided according to their cholesterol and triglyceride levels. In the study, cholesterol levels up to 200 mg/dl and triglyceride levels up to 150 mg/dl were considered as normal, and cholesterol levels of 201-239 mg/dl and of triglyceride levels of 151-200 mg/dl were considered to be moderately high. While, cholesterol levels of >239 mg/dl and triglyceride levels of >200 mg/dl were considered to be very high levels. A comparison study was conducted on the effect of the elevated level of each of the parameters (cholesterol and triglyceride) on glucose elevation as follows:
Study 1- measured the number of cases of high serum glucose >110 mg/dl between the three different serum cholesterol and triglyceride groups; 1) triglyceride 200 mg/dl, cholesterol>239 mg/dl. Study 2- measured the number of cases of high serum glucose >110 mg/dl between the two different serum cholesterol and triglyceride groups; 1) triglyceride 200 mg/dl, and 2) triglyceride >150 mg/dl, cholesterol>200 mg/dl. Study 3- measured the number of cases of high serum glucose >110 mg/dl between the two different serum cholesterol and triglyceride groups; 1) triglyceride >150 mg/dl, cholesterol 150 mg/dl, cholesterol >200 mg/dl. Study 4- measured the number of cases of high serum glucose > 110 mg/dl between the two different serum cholesterol and triglyceride groups; 1) triglyceride 200 mg/dl, and 2) triglyceride >150 mg/dl, cholesterol<201 mg/dl. Study 5- measured the glucose mean and standard deviation in the following categories; 1) Individuals with normal triglyceride normal cholesterol, 2) High triglyceride normal cholesterol, 3) Normal triglyceride high cholesterol, and 4) High triglyceride high cholesterol. Study 6- measure both the correlation and the regression considering cholesterol as the independent variable and glucose as the dependant variable. Study 7- assessed both the correlation and the regression considering triglyceride as the independent variable and glucose as the dependant variable.
The Chi-Square test was used as a means of comparing the results according to the following null hypotheses; the total number of elevated cases of glucose values >110 mg/dl between the different study groups is ≤0.05 level of significance. Thus there is no significant difference in levels of elevated glucose level among the different study groups. (-) Measuring the number of cases of high serum glucose > 110 mg/dl between groups: 1-(triglyceride 200 mg/dl), and 2- (triglyceride >150 mg/dl, cholesterol >200 mg/dl).
| Cholesterol Triglyceridemg /dl | Total number of cases studied | Number of High glucose cases >110 mg/dl | Expected # of cases with Glucose >110 mg/dl | Chi-Square value |
|---|---|---|---|---|
| Cho<201 Tg<151 | 160 | 27 | 36 | 12.45 |
| Cho 201-239 Tg 151-200 | 46 | 12 | 10 | |
| Cho>239 Tg>200 | 21 | 12 | 5 |
Measuring the number of cases of high serum glucose > 110 mg/dl between groups: 1-(triglyceride 200 mg/dl), 2- (triglyceride >150 mg/dl, cholesterol <201 mg/dl).
| Cholesterol Triglyceridemg /dl | Total number of cases studied | Number of High glucose cases >110 mg/dl | Expected # of cases with Glucose >110 mg/dl | Chi-Square value |
|---|---|---|---|---|
| Cho 150 | 81 | 38 | 28 | 7.27 |
| Cho>200 Tg <151 | 77 | 17 | 27 |
The alternative hypotheses considered the total number of elevated cases of glucose values >110 mg/dl between the different study groups is not ≤0.05 level of significance. Thus, there is a significant difference in elevated glucose levels among the different study groups in such case. In this study, we reveal the influence of both elevated serum triglyceride and cholesterol levels on glucose levels in the blood by examining the effect of elevation in both triglyceride and cholesterol on glucose, (). The results indicate that 27/160 patients in Group 1 (patients with triglyceride 200 mg/dl and >239 mg/dl respectively in Group 3, 12/21 patients were found to be hyperglycemic, ( p ≤0.05), thus there was a significant difference between the number of cases with high glucose values (>110 mg/dl)among the three study groups. () The effects of triglyceride elevations in the presence of normal cholesterol levels were compared with the effects of both high cholesterol and high triglyceride in, The results indicate that 17/77 patients in Group 1 (patients with triglyceride 201 mg/dl) were hyperglycemic. While in Group 2 (triglyceride >151 mg/dl and cholesterol >201 mg/dl), 51/120 patients were hyperglycemic, ( p ≤0.05), hence there is a significant difference in the number of cases with high glucose values >110 mg/dl between the two study groups. Measuring the number of cases of high serum glucose > 110 mg/dl between groups: 1-(triglyceride 200 mg/dl), and 2- (triglyceride >150 mg/dl, cholesterol >200 mg/dl).
| Cholesterol Triglyceridemg /dl | Total number of cases studied | Number of High glucose cases >110 mg/dl | Expected # of cases with Glucose >110 mg/dl | Chi-Square value |
|---|---|---|---|---|
| Cho>200 Tg<151 | 77 | 17 | 27 | 6.133 |
| Cho>200 Tg >150 | 120 | 51 | 41 |
shows the effect of cholesterol elevation on normal triglyceride and compares it with the effects of both high cholesterol and high triglyceride. In Group 1 (triglyceride >151 mg/dl and cholesterol 151 mg/dl and cholesterol >201 mg/dl), 51/120 patients were also in were hyperglycemic, ( p ≤ 0.05), hence there was no significant difference in the number of cases with high glucose values > 110 mg/dl between the two study groups. Measuring the number of cases of high serum glucose > 110 mg/dl between groups: 1-(triglyceride >150 mg/dl, cholesterol 150 mg/dl, cholesterol >200 mg/dl).
| Cholesterol Triglyceridemg /dl | Total number of cases studied | Number of High glucose cases >110 mg/dl | Expected # of cases with Glucose >110 mg/dl | Chi-Square value |
|---|---|---|---|---|
| Cho 150 | 81 | 38 | 36 | 0.1865 |
| Cho>200 Tg >150 | 120 | 51 | 53 |
This study also compares the effects of high triglyceride/normal cholesterol levels with the effects of high cholesterol/normal triglyceride on the levels of high glucose concentrations in the blood. The results showed that 17/77 patients in Group 1 with (triglyceride 201 mg/dl) were hyperglycemic. While in Group 2 (triglyceride >151 mg/dl and cholesterol <201 mg/dl), 38/81 patients in were also hyperglycemic, ( p ≤ 0.05). Hence, there was a significant difference in the number of cases with high glucose values >110 mg/dl between the two study groups. () Meanwhile, the mean and standard deviations were evaluated and found that in the 160 patients with normal triglyceride (<151 mg/dl) and normal cholesterol (<201 mg/d), the average glucose value was 102.89 mg/dl and the standard deviation was 40.88. The study also revealed that in the 81 patients with high triglyceride (>151 mg/dl) and normal cholesterol ( 201 mg/d), the average glucose value was 106.0 mg/dl and the standard deviation was 37.29. Also, of the 120 patients with high triglyceride (>151 mg/dl) and high cholesterol (>201 mg/d), the average glucose value was 125.33 mg/dl and the standard deviation was 46.77. () Measuring the glucose mean and standard deviation under the following categories: 1- Normal triglyceride normal cholesterol.2- High triglyceride normal cholesterol.3- Normal triglyceride high cholesterol.4- High triglyceride high cholesterol.
| Glucose | Normal triglyceride <151 mg/dlNormal cholesterol <201 mg/dl | High triglyceride >150 mg/dl normal cholesterol >200 mg/dl | Normal triglyceride high cholesterol | High triglyceride high cholesterol |
|---|---|---|---|---|
| # of patients | 160 | 81 | 77 | 120 |
| Average | 102.8863 | 128.4568 | 106.0065 | 125.3292 |
| STD | 40.88006 | 63.45413 | 37.28786 | 46.77101 |
Furthermore, shows the presence of any correlation and hence, the regression considering the cholesterol as the independent variable and the glucose as the dependant variable. The correlation coefficient value was 0.35 for all the 438 study participants.
While in patients with normal cholesterol ( 239 mg/dl), the correlation coefficient value was 0.28. Likewise, in evaluating the presence of any correlation and hence, the regression considering the triglyceride as the independent variable and the glucose as the dependant variable, the correlation coefficient value was 0.095 for all the 438 studied patients.
() Measuring both the correlation and the regression considering the cholesterol as the independent variable and the glucose as the dependant one.
| All the 438 individuals | Cholesterol is normal<201 mg/dl | Cholesterol is 201-239: mg/dl | Cholesterol is >239 mg/dl | |
|---|---|---|---|---|
| Correlation | 0.35 | 0.4 | 0.4 | 0.28 |
| Regression P (slope) | 0.19 | 0.28 | 0.116 | 0.27 |
| S y.x (Standard error of estimate) | 45.06 | 71.35 | 32.01 | 56.91 |
| S b (Estimated standard error value | 10.48 | 10.17 | 3.2 | 7.0 |
| TR (The test ratio) | 0.018 | 0.028 | 0.036 | 0.038 |
Measuring both the correlation and the regression considering the triglyceride as the independent variable and the glucose as the dependant one.
| Variables | All the 438 individuals | Triglyceride is normal<151 mg/dl | Triglyceride is 151-200 mg/dl | Triglyceride is >200mg/dl |
|---|---|---|---|---|
| Correlation | 0.095 | 0.075 | 0.040 | 0.043- |
| Regression P (slope) | 0.12 | 0.089 | 0.045 | -0.06 |
| S y.x (Standard error of estimate) | 47.93 | 39.67 | 41.41 | 44.34 |
| S b (Estimated standard error value | 26.34 | 18.37 | 11.17 | 13.5 |
| TR (The test ratio) | 0.0045 | 0.0050 | 0.0038 | -0.0045 |
In both and, the t test studied the regression slope at 5% levels of significance under the assumption that the slope of the samples according to the different categories presented above is zero. In the triglyceride case, the test ratio for the t test for the slope (TR) in all the different categories was <0.04, which is very small to reject our assumption. Thus, in all the cases, we accept our hypothesis that no true relationship exists between the elevation in serum triglyceride and the elevations in serum glucose in the same sample according to, In other words, in each and every single sample, elevation sin triglyceride does not necessarily, in the same manner, associate with the same level of glucose elevation when the test is performed on the same sample from the same patient. Likewise, according to, no true forward or reverse relationship exists between the elevation in serum cholesterol and the elevation in serum glucose in every single sample when the test is performed on the same sample from the same patient. This means that high level of cholesterol does not have to be associated with the same high glucose levels in the same sample. This retrospective study aims to further identify the real effect of elevation of serum triglyceride and serum cholesterol separately or in combination, on glucose levels in the blood. The results in reveals that the elevations in both triglyceride and cholesterol simultaneously have a strong impact and association with increasing levels of glucose in the blood and thus has a strong effect on diabetes. The results in declare that the difference is significant and hence the elevation in cholesterol alone does not have the same impact of association of both triglyceride and cholesterol elevation on increasing levels of high glucose in the blood. While the results in show no significant difference between the triglyceride elevation alone and the elevations in both triglyceride and cholesterol. Thus we conclude that elevation in triglyceride but not cholesterol has the same effect of both triglyceride and cholesterol elevation on the association with increasing cases of high glucose in blood. That last statement is confirmed by the results in, which shows a significant difference between triglyceride elevations compared to the cholesterol elevations on the number of cases with high glucose levels in the blood. Therefore, triglyceride elevation has more impact than cholesterol on levels of blood glucose elevation. By evaluating the average serum glucose values under the four categories; normal triglyceride/ cholesterol, normal triglyceride/high cholesterol, high triglyceride/normal cholesterol, high triglyceride/high cholesterol, () it is clear from the results that the average glucose value in the first and second categories did not exceed the normal glucose range, while it exceeded the normal value when serum triglyceride was elevated alone or together with cholesterol. Finally, the correlation and regression values clearly demonstrate that cholesterol is more positively correlated with glucose when compared with triglyceride, as is evident from the cholesterol correlation coefficient values, which varied between 0.28 and 0.4 among the four different study groups. The correlation coefficient values for the triglyceride with glucose only varied between -0.043 and 0.095. (-) Upon testing the hypothesis on the existence of a real forward or inverse relationship between the triglyceride and glucose or between cholesterol and glucose for example, when one value of triglyceride increases or decreases, the corresponding glucose value also responds in the same direction, we found that the TR value (the test ratio for the t test for slope) for the cholesterol groups ranged between 0.018 and 0.038 and for the triglyceride groups between - 0.0045 and 0.0045. In both cases, the values are far below the boundaries of rejection, therefore, we accept our hypothesis (the value of B which is the slope of each tested sample regression line is 0) that there is no forward or inverse relationship exists between serum triglyceride and serum glucose as a value to value, in the same sample in one hand or between serum cholesterol and serum glucose as a value to value, in the same sample in the other hand. Overall, there seems to be a strong relationship between both serum triglyceride and cholesterol elevation together and the increase levels of high blood glucose. An association was also observed between serum triglyceride elevation and the increase in high blood glucose levels. However, there was no association between serum cholesterol elevation and increases in high blood glucose. A slight correlation exists between serum cholesterol elevation and glucose elevation that are determined from the same sample. While no correlation exists between the elevation of serum triglyceride value and serum glucose value, which are determined from the same sample. Finally, no forward or inverse relationship exists between serum triglyceride and serum glucose which are determined from the same sample. The same applies for the cholesterol, as no forward or inverse relationship exists between serum cholesterol and serum glucose, which are determined from the same sample. The authors reported no conflict of interest and no funding was received on this work.1. Roman SH, Harris MI. Management of diabetes mellitus from a public health perspective. Endocrinol Metab Clin North Am 1997. Sep; 26 ( 3 ):443-474 10.1016/S0889-8529(05)70260-7 2. Harris MI. Health care and health status and outcomes for patients with type 2 diabetes. Diabetes Care 2000. Jun; 23 ( 6 ):754-758 10.2337/diacare.23.6.754 3. Briones ER, Steiger DL, Palumbo PJ, O'Fallon WM, Langworthy AL, Zimmerman BR, et al. Sterol excretion and cholesterol absorption in diabetics and nondiabetics with and without hyperlipidemia. Am J Clin Nutr 1986. Sep; 44 ( 3 ):353-361 4. O'Brien T, Nguyen TT, Zimmerman BR. Hyperlipidemia and diabetes mellitus. Mayo Clin Proc 1998. Oct; 73 ( 10 ):969-976 10.4065/73.10.969 5. Bonanome A, Visonà A, Lusiani L, Beltramello G, Confortin L, Biffanti S, et al. Carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus: effects of a low-fat, high-carbohydrate diet vs a diet high in monounsaturated fatty acids. Am J Clin Nutr 1991. Sep; 54 ( 3 ):586-590 6. Poitout V, Robertson RP. Minireview: Secondary beta-cell failure in type 2 diabetes–a convergence of glucotoxicity and lipotoxicity. Endocrinology 2002. Feb; 143 ( 2 ):339-342 10.1210/en.143.2.339 7. Hollister LE, Overall JE, Snow HL. Relationship of obesity to serum triglyceride, cholesterol, and uric acid, and to plasma-glucose levels. Am J Clin Nutr 1967. Jul; 20 ( 7 ):777-782. Printed in L.S.A.8. Menik HL, Sammanthi JS, Priyantha WT. et-al. Genetic Association Between Insulin Resistance And Total Cholesterol In Type 2 Diabetes Mellitus - A Preliminary Observation. Online J Health Allied Scs.2005; 1 :4 9. Meludu SC, Asomgha L, Dioka EC, Osuji C, Agbasi AC, Ifeanyichukwu M, et al. Exercise performance in relation to glucose drink and their effect on some biochemical parameters. Niger J Physiol Sci 2005. Jun-Dec; 20 ( 1-2 ):43-47 10. Siraja ES, Seyoumb B, Saenzc C, Abdulkadird J. Lipid and lipoprotein profiles in Ethiopian patients with diabetes mellitus. Metabolism 2006; 55 ( 6 ):706-710,10.1016/j.metabol.2005.08.002 11. Al-Nuaim AR. Effect of overweight and obesity on glucose intolerance and dyslipidemia in Saudi Arabia, epidemiological study. Diabetes Res Clin Pract 1997; 36 ( 3 ):181-191,10.1016/S0168-8227(97)00041-7 : A Study Measuring the Effect of High Serum Triglyceride and Cholesterol on Glucose Elevation in Human Serum
Does a lipid test check for diabetes?
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- The Lipid and Glucose Test has a fasting requirement of 9-12 hours prior to having your blood drawn.
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Are lipids made up of sugars?
Science >> Biology for Kids What are lipids? Lipids are one of the four major groups of organic molecules; the other three being proteins, nucleic acids (DNA), and carbohydrates (sugars). Lipids are made up of the same elements as carbohydrates: carbon, hydrogen, and oxygen. However, lipids tend to contain many more hydrogen atoms than oxygen atoms. Lipids include fats, steroids, phospholipids, and waxes. One main characteristic of lipids is that they do not dissolve in water. What do they do? Lipids play an important role in living organisms. Some of their main functions include energy storage, hormones, and cell membranes. Types of Lipids Fats
What are fats? Fats are composed of a glycerol molecule and three fatty acid molecules. Just like all lipids, fat molecules are made up of the elements carbon, hydrogen, and oxygen. Fat is used as energy storage in our bodies. Are all fats bad? No, as a matter of fact, fats are needed by our bodies to be healthy. We couldn’t live without some fats in our diet. Most people need to get around 20%-30% of their food from fats. However, too much fat can be bad for you. It can cause you to be overweight and clog up your arteries. Types of Fats There are two main types of fats: saturated fats and unsaturated fats.
Saturated Fats – Saturated fats are solids at room temperature. These fats tend to come from foods like red meat, cheese, and butter. Saturated fats are sometimes called “bad” fats because they have been known to cause higher cholesterol, clog arteries, and even increase the risk for some cancers. Unsaturated Fats – Unsaturated fats are liquids at room temperature. These fats tend to come from foods like nuts, vegetables, and fish. Unsaturated fats are considered much better for you than saturated fats and are sometimes called “good” fats.
Waxes Waxes are similar to fats in their chemical make up, however they only have one long fatty acid chain. Waxes are soft and plastic at room temperatures. They are produced by animals and plants and are typically used for protection. Plants use waxes to help prevent water loss.
Humans have wax in our ears to help protect our eardrums. Steroids Steroids are another major group of lipids. Steroids include cholesterol, chlorophyll, and hormones. Our bodies use cholesterol to make the hormones testosterone (male hormones) and estrogen (female hormones). Chlorophyll is used by plants to absorb light for photosynthesis.
Are steroids bad for you? Not all steroids are bad. Our bodies need steroids like cholesterol and cortisol to survive, so some steroids are good for us. There are also many steroids that doctors use to help sick people. However, the type of steroids you hear about in sports, anabolic steroids, can be very bad for you.
They can cause all sorts of damage to your body including strokes, kidney failure, blood clots, and liver damage. Phospholipids Phospholipids make up the fourth major group of lipids. They are very similar to fats in their chemical make up. Phospholipids are one of the main structural components of all cell membranes.
Interesting Facts about Lipids
When a compound is not water soluble it is called “hydrophobic.” Honeybees use wax to make their honeycombs. Waxes are used in all sorts of everyday applications including chewing gum, polishes, and candles. Fats help us to dissolve and store some important vitamins including A, D, E, and K. Cortisol is a type of steroid that our bodies use to regulate energy and fight off diseases.
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Do lipids come from glucose?
Triglycerides – Triglycerides, a form of long-term energy storage in animals, are made of glycerol and three fatty acids. Animals can make most of the fatty acids they need. Triglycerides can be both made and broken down through parts of the glucose catabolism pathways.
- Glycerol can be phosphorylated to glycerol-3-phosphate, which continues through glycolysis.
- Fatty acids are catabolized in a process called beta-oxidation that takes place in the matrix of the mitochondria and converts their fatty acid chains into two carbon units of acetyl groups, while producing NADH and FADH 2,
The acetyl groups are picked up by CoA to form acetyl CoA that proceeds into the citric acid cycle as it combines with oxaloacetate. The NADH and FADH 2 are then used by the electron transport chain.