How Obesity Causes Diabetes?

How Obesity Causes Diabetes
Conclusion – Diabetes and obesity are chronic disorders that are on the rise worldwide. Body mass index has a strong relationship to diabetes and insulin resistance. In an obese individual, the amount of NEFA, glycerol, hormones, cytokines, proinflammatory substances, and other substances that are involved in the development of insulin resistance are increased.

Why does obesity cause insulin resistance?

Abstract – Obesity is a triggering factor for diabetes associated with insulin resistance. In individuals who are obese, higher amounts of non-esterified fatty acids, glycerol, hormones, and pro-inflammatory cytokines that could participate in the development of insulin resistance are released by adipose tissue.

  1. Besides, endoplasmic reticulum stress, adipose tissue hypoxia, oxidative stress, lipodystrophy, and genetic background have a role in insulin resistance.
  2. However, no effective drug therapy was developed for type 2 diabetes mellitus targeting these physiological factors.
  3. This is might be due to a lack of agreement on the comprehensive mechanism of insulin resistance.

Therefore, this review assesses the cellular components of each physiologic and pathophysiologic factors that are involved in obesity associated insulin resistance, and may encourage further drug development in this field. Keywords: obesity, insulin, insulin resistance, type 2 diabetes mellitus

How does obesity increase the risk of type 2 diabetes?

What are Obesity Types? – Obesity and Type 2 Diabetes There are many risk factors for type 2 diabetes, including age, race, pregnancy, stress, certain medications, genetics or family history, and high cholesterol. However, one of the best predictors of type 2 diabetes? Being overweight or obese.

Almost 90% of people with type 2 diabetes are overweight or obese. But, why? Well, obesity causes increased levels of fatty acids and inflammation, leading to insulin resistance, which in turn can lead to type 2 diabetes. Type 2 diabetes, known as non-insulin dependent diabetes, is the most common form of diabetes and accounts for approximately 90% of diabetes cases.

People with type 2 diabetes can produce some of their own insulin, but it’s often not enough or the body’s cells don’t respond to it. As a result of this insulin resistance, glucose (blood sugar) builds up in the body, leading to high blood sugar. Patients with high blood sugar will typically experience frequent urination, increased thirst, and increased hunger.

  1. Fatigue may also result from dehydration.
  2. Untreated or poorly controlled diabetes can cause other health concerns like vision problems, nerve damage, infections, heart problems, high blood pressure, mental health issues, ketoacidosis, and stroke.
  3. Since there is an association between type 2 diabetes and being overweight, treatment for type 2 diabetes often focuses on diet and exercise.

Oral medications can also help the body use its own insulin more efficiently. In some cases, insulin injections are necessary to normalize blood sugars. Living with Obesity and Type 2 Diabetes Living with obesity and type 2 diabetes is not without its risks, but there’s a lot you can do to take charge of your health.

Managing diabetes includes eating healthy foods, exercising regularly, reducing stress, maintaining a healthy lifestyle, and, at the advice of your doctor, using medications. While Type 2 diabetes can be treated, it is largely preventable. Lifestyle changes and small amounts of weight loss can help reduce the risk of developing diabetes by 40-60%.

Interested in learning the optimal diet, exercise, and supplementation for diabetes? Order a Health + Ancestry Report and learn how to diet, exercise. and supplement right for your DNA and lifestyle.

How does obesity impact insulin?

Abstract – Obesity-associated insulin resistance is a major risk factor for type 2 diabetes and cardiovascular disease. In the past decade, a large number of endocrine, inflammatory, neural, and cell-intrinsic pathways have been shown to be dysregulated in obesity.

  • Adipocyte
  • adipokines
  • diabetes
  • insulin resistance
  • obesity
  • signaling

The number of obese individuals worldwide has reached 2.1 billion, leading to an explosion of obesity-related health problems associated with increased morbidity and mortality ( Li et al.2005 ; Olshansky 2005 ). Obese individuals develop resistance to the cellular actions of insulin, characterized by an impaired ability of insulin to inhibit glucose output from the liver and to promote glucose uptake in fat and muscle ( Saltiel and Kahn 2001 ; Hribal et al.2002 ).

  • Insulin resistance is a key etiological factor for type 2 diabetes mellitus (T2DM), which has reached epidemic proportions: In the United States, ∼6% of the current adult population is diagnosed with this disease.
  • An additional 41 million people are prediabetic, with a constellation of insulin resistance, hypertension, and dyslipidemia that puts them at increased risk for cardiovascular morbidity and mortality ( Zimmet et al.2001 ; American Diabetes Association diabetes statistics at http://www.diabetes.org/diabetes-statistics/prevalence.jsp ).

Lifestyle changes, while desirable, have proven difficult to achieve. Thus, a better understanding of the molecular mechanisms underlying insulin resistance will be required to combat the epidemics of T2DM and cardiovascular disease that are fueled by obesity-associated insulin resistance.

The association between obesity and insulin resistance is likely a cause-and-effect relationship since human and animal studies indicate that weight loss/gain correlates closely with increasing/decreasing insulin sensitivity, respectively ( Sims et al.1973 ; Freidenberg et al.1988 ; Bak et al.1992 ).

In this review, we explore current ideas of how increased adipose mass predisposes to systemic insulin resistance, focusing on dysregulation of interconnected endocrine, inflammatory, neural, and cell-autonomous pathways.

How does obesity affect glucose metabolism?

With obesity there is reduced glucose disposal in adipose tissue. It has been suggested that obesity leads to the development of hyperglycemia, hyperlipemia, hyperinsulinemia, and insulin resistance.

Is obesity the main cause of type 2 diabetes?

Abstract – Obesity is believed to be a promoter of type 2 diabetes mellitus (T2DM). Reports indicate that severe obesity in childhood and adolescence increases the risk of T2DM in youth and young adults. T2DM, which is commonly asymptomatic, frequently is not recognized until random blood glucose is measured.

Screening blood glucose levels measured in obese individuals are more effective for identifying undiagnosed persons, than screening the general population and therefore introduces a selection bias for discovery. The following commentary will indicate why these observations do not indicate that obesity is the cause of T2DM.

Also, it will be shown that the insulin resistance of T2DM occurs primarily in the muscles of lean individuals predisposed to diabetes before they become obese. This insulin resistance is not secondary to, but instead, is the cause of the excessive fat accumulation associated with T2DM.

Do all obese people get type 2 diabetes?

Conclusions: – The major questions linking obesity to type 2 diabetes that need to be addressed by combined basic, clinical, and population-based scientific approaches include the following: 1 ) Why do not all patients with obesity develop type 2 diabetes? 2 ) Through what mechanisms do obesity and insulin resistance contribute to β-cell decompensation, and if/when obesity prevention ensues, how much reduction in type 2 diabetes incidence will follow? 3 ) How does the duration of type 2 diabetes relate to the benefits of weight reduction by lifestyle, weight-loss drugs, and/or bariatric surgery on β-cell function and glycemia? 4 ) What is necessary for regulatory approval of medications and possibly surgical approaches for preventing type 2 diabetes in patients with obesity? Improved understanding of how obesity relates to type 2 diabetes may help advance effective and cost-effective interventions for both conditions, including more tailored therapy. To expedite this process, we recommend further investigation into the pathogenesis of these coexistent conditions and innovative approaches to their pharmacological and surgical management. Most patients with type 2 diabetes are obese, and the global epidemic of obesity largely explains the dramatic increase in the incidence and prevalence of type 2 diabetes over the past 20 years. Currently, over a third (34%) of U.S. adults are obese (defined as BMI >30 kg/m 2 ), and over 11% of people aged ≥20 years have diabetes ( 1 ), a prevalence projected to increase to 21% by 2050 ( 2 ). However, the precise mechanisms linking the two conditions remain unclear, as does our understanding of interindividual differences. Improved understanding will help advance identification and development of effective treatment options. Excess weight is an established risk factor for type 2 diabetes, yet most obese individuals do not develop type 2 diabetes. Recent studies have identified “links” between obesity and type 2 diabetes involving proinflammatory cytokines (tumor necrosis factor and interleukin-6), insulin resistance, deranged fatty acid metabolism, and cellular processes such as mitochondrial dysfunction and endoplasmic reticulum stress. These interactions are complex, with the relative importance of each unclearly defined. Further genetic studies may elucidate additional common pathophysiological pathways for obesity and diabetes and identify promising new treatment targets. As physicians frequently prescribe glucose-lowering medications associated with weight gain, trade-offs between glycemic control and body weight with current therapeutic options need more consideration. This issue is particularly pressing given accumulating evidence that even modest weight reduction—whether through lifestyle/behavioral interventions, obesity medications, or bariatric surgery—can improve glycemic control and reduce diabetes risk. These intriguing, but still largely unexplored, connections between obesity and type 2 diabetes suggested the timely need to convene a group of scientific experts in the fields to more closely examine underlying pathophysiology and treatment options for patients with type 2 diabetes addressing issues of excess weight and glycemic control simultaneously. Participants in the January 2011 conference (see Appendix) were tasked with examining what is known about the relationship between obesity and type 2 diabetes and the heterogeneity of these conditions, what needs to be learned, and how to direct future research in these areas to advance effective interventions and improve patient care. What follows summarizes the major issues addressed and the outcomes of the discussion.

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Does eating fat cause diabetes?

Skip Nav Destination Article navigation Editorial | March 01 2002 Julie A. Marshall, PHD ; From the University of Colorado Health Sciences Center, Denver, Colorado Search for other works by this author on: Daniel H. Bessesen, MD From the University of Colorado Health Sciences Center, Denver, Colorado Search for other works by this author on: Diabetes Care 2002;25(3):620–622 The recent release of results from the Finnish Diabetes Prevention Study (FDPS) (1) and the Diabetes Prevention Program (DPP) (2) strongly confirm the hypothesis that interventions that alter diet and physical activity to achieve weight loss can prevent or postpone the development of type 2 diabetes in high-risk individuals.

The next challenge will be to translate these impressive results into clinical practice. It seems relevant in this context to ask, “What is the best dietary intervention strategy to improve insulin action and prevent diabetes?” In the current issue of Diabetes Care, van Dam et al. (3) assess the association between diet and development of diabetes over a 12-year period in the Health Professionals Follow-up Study (HPFS).

They find that consumption of a high-fat diet and high intakes of saturated fat are associated with an increased risk of type 2 diabetes. However, this association disappears when they adjust for BMI. They also find that frequent consumption of processed meats is associated with an increased risk for diabetes.

Can obesity cause high insulin levels?

The significance of the location of body fat for insulin resistance. – The relationship between obesity and insulin resistance is seen across all ethnic groups and is evident across the full range of body weights. Large epidemiologic studies reveal that the risk for diabetes, and presumably insulin resistance, rises as body fat content (measured by body mass index ) increases from the very lean to the very obese, implying that the “dose” of body fat has an effect on insulin sensitivity across a broad range ( 27 ).

  • Although this relationship is seen with measures of adiposity such as BMI, which reflect general adiposity, it is critical to realize that all sites of adiposity are not equal in this regard.
  • Central (intra-abdominal) depots of fat are much more strongly linked to insulin resistance, type 2 diabetes, and cardiovascular disease than are peripheral (gluteal/subcutaneous) fat depots ( 28 ).

This fact about fat and insulin sensitivity has not been adequately explained. It is possible that an unknown common factor, either genetic or environmental, produces both insulin resistance and the central pattern of regional adiposity, and that central obesity does not actually cause insulin resistance.

Alternatively, some biochemical feature of intra-abdominal adipocytes may directly influence systemic insulin sensitivity. A leading hypothesis in this regard is that intra-abdominal adipocytes are more lipolytically active, in part due to their complement of adrenergic receptors. This would increase intraportal FFA levels and flux, which might inhibit insulin clearance and promote insulin resistance by mechanisms that are still uncertain.

Hyperinsulinemia per se can cause insulin resistance by downregulating insulin receptors and desensitizing postreceptor pathways, as was confirmed by overexpression of insulin in livers of otherwise normal transgenic mice. This transgene resulted in an age-related reduction in insulin receptor expression, glucose intolerance, and hyperlipidemia without any primary genetic defect in insulin action or secretion (reviewed in ref.29 ).

Do obese people have high insulin?

2.1.4 Laboratory procedures – Plasma glucose, plasma FFA and blood tests – Plasma glucose measurement during the OGTT (Visit-2, arterialized venous plasma from the forearm), and in the morning at Visit-1 and Visit-3 (capillary plasma glucose) was analysed with HemoCue® Glucose 201 + (Hemocue AB, Ängelholm, Sweden, estimated mean coefficient of variation (CV) of 2.4%). Plasma free fatty acid (FFA) analyses were performed with an enzymatic colorimetric method at the Department of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden. The CV for the method is 4.0%. Other analyses performed at the accredited laboratory at Department of Clinical Chemistry, Sahlgrenska University Hospital were measurements of blood samples from the screening visit (Supplemental Material). Insulin and inulin measurements in dialysates, serum and plasma – At Visit-1, serum insulin was analysed for the non-T2D participants at an accredited laboratory at the Department of Clinical Chemistry, Sahlgrenska University Hospital. All measurements of serum insulin during Visit-2 were performed at the Wallenberg laboratory with the Mercodia Insulin ELISA assay (Mercodia AB, Uppsala, Sweden). The intra-assay and in between-assay CV for this method were 3.4% and 4.5%, respectively. The detection limit of the Mercodia ELISA kit was 3 mU/l and the cross-reactivity with proinsulin was <0.01%. Dialysate insulin was measured using an ultrasensitive enzyme immunoassay method (Mercodia Ultrasensitive Insulin ELISA, Mercodia AB, Uppsala, Sweden). The intra-assay and in between-assay CV for this method were 5.3% and 6.0%, respectively. The detection limit of the Ultrasensitive Mercodia ELISA kit was 0.15 mU/l and the cross-reactivity with proinsulin was <0.01%. Dialysate and plasma inulin were measured by a photometric method. The intra-assay CV for inulin was estimated to be approximately 10%. We used the external reference technique with inulin

  • Sjostrand M.
  • Holmang A.
  • Lonnroth P.

Measurement of interstitial insulin in human muscle. ] (Inutest®, 0.25 g/ml, Fresenius Kabi Austria GmbH, Linz, Austria) to determine recovery for insulin in situ, The recovery of insulin in subcutaneous adipose tissue was (4±3, 3±3, 4±2 %, mean±SD) in lean, obese-IR and obese-T2D participants, respectively.

Glycerol, lactate and glucose measurements in dialysates and plasma – Dialysate glycerol, lactate, glucose and plasma glycerol and lactate, were analysed with an enzymatic colorimetric method, sample volume 0.2 µl, using a CMA 600 Microdialysis analyser (MDialysis AB, Stockholm, Sweden) (CV of 2.0, 4.4 and 3.9% for measurements in dialysates, and 1.4, 10.4, 7.6% for measurements in plasma, for glucose, lactate and glycerol, respectively).

The endogenous reference technique

  • Strindberg L.
  • Lonnroth P.

Validation of an endogenous reference technique for the calibration of microdialysis catheters. ] includes urea and is used for calculation of recovery for glucose, lactate and glycerol, thereby enabling assessment of their absolute concentration in the interstitial fluid in subcutaneous adipose tissue.

We assessed the relative recovery for every metabolite (glucose: 39±16, 25±7, 34±10%; lactate: 36±10, 22±5, 29±9%; glycerol: 42±11, 25±6, 33±10%) in lean, obese-IR and obese-T2D participants, respectively (Supplemental Material). Total RNA extraction and quantitative PCR gene-expression analysis – RNA was obtained from adipose tissue by the guanidinium–thiocyanate extraction method.

cDNA was prepared using the ImProm-II™ Reverse Transcriptase (Promega, A3803), and qPCR was performed using the commercial SsoAdvanced™ Universal SYBR® Green Supermix (Bio-Rad 172-5274). Primer sequences are listed in Supplemental material. RNA sequencing of adipose tissue – RNA concentration was measured using Nanodrop.

Quality of RNA was evaluated using Tapestation 2200 (Agilent). Library preparation was performed using TruSeq Stranded Total RNA Sample Preparation Kit with Ribo-Zero Gold (Illumina). The pool of 25 samples was sequencing twice on a NextSeq500 instrument (Illumina) with Nextseq500 Kit High Output V2 reagent (Illumina), read length 2*75, and loading concentration 1,45pM.

RNA sequencing data analyses – For every sample, at least 35 million reads were sequenced. Raw sequence files were subjected to quality control analysis using FastQC (v 1.3) ( http://www.bioinformatics.babraham.ac.uk/projects/fastqc/, accessed on May 2020).

  • Dobin A.
  • Davis C.A.
  • Schlesinger F.
  • Drenkow J.
  • Zaleski C.
  • Jha S.
  • et al.

STAR: ultrafast universal RNA-seq aligner. ] (assigned to a gene using the GENCODE annotation (v27) using the STAR function “quantMode GeneCounts”) mapped to the human genome version GRCh38 and with reference annotation. Read counts generated by STAR were analysed by using DESeq2 package

  • Love M.I.
  • Huber W.
  • Anders S.

Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. ] for detecting genes that were differentially expressed. An adjusted p-value cut off of 0.05 was decided as threshold for detection of DEGs. Starting from the expression matrix, genes that were considered as differentially regulated, were analysed using hierarchical clustering method (Cluster 3.0, http://bonsai.hgc.jp/~mdehoon/software/cluster/software.htm, accessed on May 2020).

  • Visualization of the clustering and heatmap of log2-normalized values were obtained using Java Treeview.
  • To explore the high-dimensional property of the data we used Principal Component Analysis (PCA), as dimensionality reduction algorithm implemented in stats package.
  • For the Functional annotations analyses we used Enrichr web tools, accessed on May 2020.

The enriched annotation table results, obtained in the web site, were then downloaded to be processed and visualized using ggplot2 package.

Do obese people have more insulin?

Understanding why some obese people stay sensitive to insulin Understanding why some obese people stay sensitive to insulin Obesity, especially central obesity, is associated with insulin resistance, which precedes diabetes, sometimes by more than a decade.

However, it’s not only a question of body weight or fat distribution, because some obese people remain insulin-sensitive, with insulin working as well in their bodies as in someone lean. https://www.garvan.org.au/news-events/news/understanding-why-some-obese-people-stay-sensitive-to-insulin https://www.garvan.org.au/news-events/news/understanding-why-some-obese-people-stay-sensitive-to-insulin/@@download/image/diabetes_sm.jpg Obesity, especially central obesity, is associated with insulin resistance, which precedes diabetes, sometimes by more than a decade.

However, it’s not only a question of body weight or fat distribution, because some obese people remain insulin-sensitive, with insulin working as well in their bodies as in someone lean. Obesity, especially central obesity, is associated with insulin resistance, which precedes diabetes, sometimes by more than a decade. However, it’s not only a question of body weight or fat distribution, because some obese people remain insulin-sensitive, with insulin working as well in their bodies as in someone lean.It also seems that in addition to having a lower risk of Type 2 diabetes than insulin-resistant people of the same weight, these insulin-sensitive obese individuals appear to have greater protection against death from cardiovascular disease,While this much is agreed, closer examination shows just how much confusion still reigns in the detail.

Even estimates of the proportion of these healthier obese people range from 2% to 30% of the obese population, depending on the definition used and the cohorts of people chosen. So say the authors of a review of 79 publications on this topic, Drs and from Sydney’s Garvan Institute of Medical Research.

Published in, the review is now online. Insulin, a hormone made by the pancreas, helps the body use glucose for energy. ‘Insulin resistance’ arises when muscle cells become less able to use insulin to take in glucose from blood. This causes the pancreas to work harder to produce more insulin.

  1. Years of overwork lead to exhaustion of insulin-producing cells, which start to die, and Type 2 diabetes develops.Dr Jerry Greenfield, Head of the Department of Endocrinology at St.
  2. Vincent’s Hospital as well as leader of a clinical research group at Garvan, is keen to delve deeper into the phenomenon of the insulin-sensitive obese, remarking “The key questions are ‘whether it will be meaningful, and, if so, how will we be able to identify these individuals in clinical practice?'””A study of these people to examine what protects them from developing diabetes could be very informative in telling us what causes insulin resistance – and in developing targeted therapies.””We’re not proposing that insulin-sensitive obese people are completely protected from developing heart disease and diabetes.
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Rather, they appear to have a lower risk of these diseases compared to someone who is insulin-resistant, yet as obese.””Our review made it clear that there is still much work to be done in establishing definitions and ensuring we are all talking about the same thing.

In my mind, the only way to be sure that one is actually dealing with a group of insulin-sensitive obese people is to compare them to a group of lean people.””We are in the process of recruiting obese people for a clinical study where we’re doing a range of tests to further study these individuals’ protective metabolic features.

I think it’s a very valuable area to study because it can inform us a lot about what causes insulin resistance.”Co-author Dr Dorit Samocha-Bonet agreed that the phenomenon should be used as a tool to investigate insulin resistance – and that future studies should define their terms more rigorously.”Some of the studies we reviewed were not optimally done – failing to match BMI and gender.

Others used different ways of measuring insulin sensitivity, making it difficult to compare apples with apples.””It’s clear that there is room for studies with better matching and better markers. Using the hyperinsulinemic euglycemic clamp for example, as we do here, is far more reflective of insulin sensitivity than using surrogate markers, such as fasting blood glucose and insulin.

“”The studies we reviewed agreed that there was less fat in the liver of the insulin-sensitive obese person, as well as fewer potentially damaging fat metabolites in muscle.” “We don’t yet have a profile of all the protective factors – and there have not been enough longitudinal studies done to show how long, or to what degree, the protection continues, although one study suggests up to 30 years.” : Understanding why some obese people stay sensitive to insulin

What is the link between sugar and obesity?

2. Impacts blood sugar and hormone levels – It’s well known that eating sugary foods significantly raises your blood sugar levels. Though enjoying a sweet food infrequently isn’t likely to harm health, daily consumption of large amounts of added sugar can lead to chronically elevated blood sugar levels,

  • Prolonged elevated blood sugar — known as hyperglycemia — can cause serious harm to your body, including weight gain ( 5 ).
  • One way hyperglycemia leads to weight gain is through promoting insulin resistance.
  • Insulin is a hormone produced by your pancreas that moves sugar from your blood into cells, where it can be used for energy.

Insulin is also involved in energy storage, telling your cells when to store energy as either fat or glycogen, the storage form of glucose. Insulin resistance is when your cells stop responding properly to insulin, which leads to elevated sugar and insulin levels.

  • High blood sugar levels impair normal cell function and promote inflammation, which increases insulin resistance, furthering this destructive cycle ( 6, 7 ).
  • Though cells become resistant to insulin’s effect on blood sugar uptake, they remain responsive to the hormone’s role in fat storing, meaning that fat storage is increased.

This phenomenon is known as selective insulin resistance ( 8, 9 ). This is why insulin resistance and high blood sugar are associated with increased body fat — specifically in the belly area ( 10, 11 ). Additionally, high blood sugar levels and insulin resistance interfere with leptin, a hormone that plays a major role in energy regulation — including calorie intake and burning — and fat storage.

How does weight affect blood glucose levels?

December 14, 2012 Dear Mayo Clinic: Can type 2 diabetes be cured just by losing weight? Answer: Losing weight can have a big impact on diabetes. Although it might not cure type 2 diabetes in every case, getting to a healthy body weight does have that potential for many people.

Even if it doesn’t completely cure the disease, losing weight may make it possible for people with diabetes to take less medication. It often helps manage or prevent some of the health problems that can come with diabetes, too. People who have diabetes have too much sugar in their blood. This happens because of a problem with the hormone called insulin.

Insulin is made in the pancreas — a gland located just behind the stomach. When you eat, the pancreas releases insulin into your bloodstream. The insulin allows sugar to enter your cells, lowering the amount of sugar in your blood. If you have type 2 diabetes, the pancreas does not make enough insulin or your body cannot use insulin as well as it should.

So sugar cannot move into your cells. Instead, it builds up in your blood. The reason why type 2 diabetes develops is not completely clear. But being overweight plays a role. In people who are overweight, the body sometimes needs as much as two to three times more insulin than it would if it was at a healthy weight.

In those who develop diabetes, that is more insulin than the pancreas is able to produce. When the pancreas tries to make that much insulin, it is pushed beyond its capacity and insulin-producing cells start to die. That makes the situation worse because the pancreas then has even fewer cells with which to make insulin.

  1. Compounding the problem, research also has shown that fat cells of people who are obese and who have more abdominal fat actually release molecules that can be harmful to the pancreas.
  2. So the more abdominal fat you have, the higher the risk of damage to your pancreas.
  3. Getting to a lower weight reduces many of these problems.

When you weigh less, your pancreas is better able to keep up with your body’s need for insulin. In some cases, weight loss is enough to restore blood sugar to a normal level, which eliminates diabetes. Even if it doesn’t get your blood sugar completely back to normal, it may lower your need for insulin therapy or other medications to control diabetes.

It also lessens your risk for other serious complications of diabetes, including heart problems, kidney disease and nerve damage. The benefits of healthy weight as it relates to diabetes continue over time, too. Many people mistakenly believe that a person’s risk for diabetes automatically goes up with age.

In fact, your diabetes risk rises over time only if you gain weight and are less active as you age. For those who stay fit, the risk of developing diabetes remains the same or increases only slightly. For those with a family history of diabetes, weight control is critical.

  • Research has shown that people who have a family history of type 2 diabetes are more vulnerable to developing type 2 diabetes themselves.
  • Staying at a healthy weight lowers their chances of getting the disease by about 70 to 90 percent.
  • In general, healthy weight is defined as a body mass index, or BMI, of 25 or lower.
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To get there, you don’t need to run marathons or do hours of workouts each day. But you do need to be active on a regular basis. If you are interested in losing weight, talk to your doctor about an exercise and diet program that best fits your needs. — Robert Rizza, M.D., and Michael Jensen, M.D., Endocrinology, Mayo Clinic, Rochester, Minn.

Why do some fat people get diabetes and others don’t?

Why Do Some People Develop Diabetes and Others Don’t? Risk factors for type 2 diabetes Why do some people develop diabetes, and others don’t? Lifestyle and environmental factors account for the majority of the diabetes epidemic. We know that an energy-dense Western-style diet (food trucks, anyone?) and a sedentary lifestyle (thanks, COVID-19 L) are responsible for the epidemic of obesity, and that obesity often leads to diabetes.

But not everyone who is obese gets diabetes, and not everyone with diabetes is obese! Why??? Genetics! Scientists have already identified 500 genes that are associated with type 2 diabetes, which together account for 20% of the predisposition to type 2 diabetes. But genes don’t explain everything. In addition to genetic factors, there are “epigenetic” factors, which are influences outside the DNA.

These include things like aging, the environment, and exposure to substances during gestation. For example, prenatal exposure to famine has been associated with a higher risk of developing type 2 diabetes. Also, the children of women who have gestational diabetes are eight times more likely to develop diabetes themselves! So, if you don’t want your baby to grow up to have diabetes, don’t get pregnant during a famine, but if you must, don’t get diabetes while you are pregnant! What are some surprising risk factors for diabetes? Many of us know about the risks incurred by lack of exercise and by drinking Mountain Dew and other sugar-sweetened beverages (e.g.

  • Sweet tea).
  • But did you know that eating a low fiber diet, not sleeping enough, and even exposure to loud road noise are all independent risk factors for diabetes? Did you know that drinking 3 or more cups of coffee (either caffeinated or decaffeinated) is associated with a lower risk of diabetes? The Microbiome One of the frontiers in diabetes risk management involves our complex intestinal ecosystem: the “gut microbiome.” The gut is nearly sterile at birth.

However, by age three, the gut has acquired most of the microbes that will be present through adulthood. These microscopic organisms (certain types of bacteria, fungi, and viruses) share a symbiotic relationship with the lining of the gut. The two main types of bacteria in the gut are called Firmicutes and Bacteroidetes.

  1. Firmicutes are found predominantly in the small intestines, while Bacteroidetes reside mostly in the colon.
  2. These bacteria are involved in nutrient metabolism, drug metabolism, maintenance of the gut lining, and protection against pathogens.
  3. Dysbiosis (an imbalance of gut microbes) occurs as a result of an unhealthy diet, antibiotic treatment, or chronic infection.

In one study, four days of a meat-based diet rapidly decreased the abundance of Firmicutes in the gut. Who would have thought that eating meat was bad for us? Also, it has been shown that the guts of patients with diabetes and prediabetes have fewer of the type of bacteria that change carbohydrates into short-chain fatty acids (SCFAs).

Can you be obese and healthy?

The relationship between health and weight is complex. The concept of weight speaks to how much your whole body weighs—your weight is comprised of not only fat/adipose tissue, but also bone, water weight, organs, skin, muscles and more. What constitutes a healthy weight is dependent on the individual.

While being overweight is a precursor to obesity and, like obesity, can increase the risk of diabetes, heart attack and stroke, it’s also possible to be overweight and still healthy, especially if you’re free from chronic diseases like hypertension or diabetes. However, it’s important to keep in mind that many studies have shown an association between excess weight and adverse health outcomes and shorter life spans, especially if your waist circumference is greater than 39 inches for men and 34 inches for women.

The way we discuss weight can further be categorized by body mass index, or BMI.

Does every obese person have insulin resistance?

More than 70% of obese population are insulin resistant. However, more than 50% of lean individuals are also accompanied with insulin-resistant status, 12 which may be even higher in lean stroke patients.

Does obesity always mean insulin resistance?

Understanding why some obese people stay sensitive to insulin Understanding why some obese people stay sensitive to insulin Obesity, especially central obesity, is associated with insulin resistance, which precedes diabetes, sometimes by more than a decade.

However, it’s not only a question of body weight or fat distribution, because some obese people remain insulin-sensitive, with insulin working as well in their bodies as in someone lean. https://www.garvan.org.au/news-events/news/understanding-why-some-obese-people-stay-sensitive-to-insulin https://www.garvan.org.au/news-events/news/understanding-why-some-obese-people-stay-sensitive-to-insulin/@@download/image/diabetes_sm.jpg Obesity, especially central obesity, is associated with insulin resistance, which precedes diabetes, sometimes by more than a decade.

However, it’s not only a question of body weight or fat distribution, because some obese people remain insulin-sensitive, with insulin working as well in their bodies as in someone lean. Obesity, especially central obesity, is associated with insulin resistance, which precedes diabetes, sometimes by more than a decade. However, it’s not only a question of body weight or fat distribution, because some obese people remain insulin-sensitive, with insulin working as well in their bodies as in someone lean.It also seems that in addition to having a lower risk of Type 2 diabetes than insulin-resistant people of the same weight, these insulin-sensitive obese individuals appear to have greater protection against death from cardiovascular disease,While this much is agreed, closer examination shows just how much confusion still reigns in the detail.

  • Even estimates of the proportion of these healthier obese people range from 2% to 30% of the obese population, depending on the definition used and the cohorts of people chosen.
  • So say the authors of a review of 79 publications on this topic, Drs and from Sydney’s Garvan Institute of Medical Research.

Published in, the review is now online. Insulin, a hormone made by the pancreas, helps the body use glucose for energy. ‘Insulin resistance’ arises when muscle cells become less able to use insulin to take in glucose from blood. This causes the pancreas to work harder to produce more insulin.

Years of overwork lead to exhaustion of insulin-producing cells, which start to die, and Type 2 diabetes develops.Dr Jerry Greenfield, Head of the Department of Endocrinology at St. Vincent’s Hospital as well as leader of a clinical research group at Garvan, is keen to delve deeper into the phenomenon of the insulin-sensitive obese, remarking “The key questions are ‘whether it will be meaningful, and, if so, how will we be able to identify these individuals in clinical practice?'””A study of these people to examine what protects them from developing diabetes could be very informative in telling us what causes insulin resistance – and in developing targeted therapies.””We’re not proposing that insulin-sensitive obese people are completely protected from developing heart disease and diabetes.

Rather, they appear to have a lower risk of these diseases compared to someone who is insulin-resistant, yet as obese.””Our review made it clear that there is still much work to be done in establishing definitions and ensuring we are all talking about the same thing.

In my mind, the only way to be sure that one is actually dealing with a group of insulin-sensitive obese people is to compare them to a group of lean people.””We are in the process of recruiting obese people for a clinical study where we’re doing a range of tests to further study these individuals’ protective metabolic features.

I think it’s a very valuable area to study because it can inform us a lot about what causes insulin resistance.”Co-author Dr Dorit Samocha-Bonet agreed that the phenomenon should be used as a tool to investigate insulin resistance – and that future studies should define their terms more rigorously.”Some of the studies we reviewed were not optimally done – failing to match BMI and gender.

  1. Others used different ways of measuring insulin sensitivity, making it difficult to compare apples with apples.””It’s clear that there is room for studies with better matching and better markers.
  2. Using the hyperinsulinemic euglycemic clamp for example, as we do here, is far more reflective of insulin sensitivity than using surrogate markers, such as fasting blood glucose and insulin.

“”The studies we reviewed agreed that there was less fat in the liver of the insulin-sensitive obese person, as well as fewer potentially damaging fat metabolites in muscle.” “We don’t yet have a profile of all the protective factors – and there have not been enough longitudinal studies done to show how long, or to what degree, the protection continues, although one study suggests up to 30 years.” : Understanding why some obese people stay sensitive to insulin

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