Program Editors Ralph Anthony DeFronzo, MD Professor of Medicine and Chief of the Diabetes Division University of Texas Health Science Center Audie L. Increasing Problem of Obesity and Diabetes: Mexico ObesityDiabetes Mexican Population (%) Aguilar-Salinas CA, et al.
Diabetes Is a Cardiovascular Disease Risk Equivalent DM=diabetes mellitus; MI=myocardial infarction.
Microvascular Disease 0 10 20 30 40 50 60 70 80 567891011 Mean HbA 1c (%) Stratton IM, et al. Optimizing Glycemia in Advanced Type 2 Diabetes Exerts Unclear Macrovascular Benefit ACCORD Study Group. In fact, the American Heart Association has now elevated overweight and obesity to risk status for heart attach, stroke, and peripheral artery disease. Upper body distribution exhibits a higher incidence of diabetes, independent of degree of obesity. Nonalcoholic Fatty Liver Disease (NAFLD) is the most common cause of liver abnormalities and clinical follow-up; including liver transplantation. The fat biopsy on the left illustrates excess and enlarged fat cell in the liver; whereas the biopsy on the right is normal hepatic (liver) tissue. As body fat increases, the intraorgan fat deposits increase similarly in children and adults who are more susceptable to metabolic syndrome and diabetes. Lipid accumulation in the cardiac tissue are associated with conduction defects as lipid can accumulate in the SA node, AV node, and right bundle branch.
Excess intramuscular fat deposits are associated with increased lipid metabolism within the muscle. Sims & colleagues compared endocrine and metabolic changes between spontaneous and experimental obestiy and found most of the changes were similar. As the size of the adipocyte grows in overweight and obesity, the endocrine activities change. The leptin resistance may be found more in the central nervous system than in the peripheral organs (pancreas, liver & muscle).
IL-6 is another cytokine secreted from the macrophage in adipose tissue and is elevated in overweight and obesity.
Substances from the renin-angiotensin system (RAS) are increased in overweight and obesity.


The increase in resistin found in overweight and obesity increases insulin resistance, leading to metabolic syndrome, diabetes and atherosclerosis.
The pathophysiology of obesity, as it relates to the etiology of atherosclerosis, metabolic syndrome and diabetes is summarized below. The adipocyte with excess lipid produces oxidative stress as represented by the increase in TNF-alpha and IL-6. Apparenlty healty adults increase oxidative stress during high intensity or maximal exericse (yellow line).
On those same lines, any physical activity for overweight and obese individuals will produce more oxidative stress than thier normal weight counterpart. This elevated oxidative stress has a role in the etiology of cardiovascular disease and cancer. Metabolic syndrome is cluster of metabolic abnormalities and cardiovascular risk factors. Nitric oxide (NO) is the molecule that protects the artery from developing atherosclerosis. The key to understanding the etiology of cancer is found in the cell cycle of the reproduction of the cell. Excess body weight requires a higher metabolic demand, not only for the adipose tissue, but for the body as a whole.
To complicate this further, remember VO2 max will be considerably lower in the overweight or obese individual, which makes the intensity, relative to their max, quite high. Excess body fat not only leads directly to modern chronic disease, but worsens the severity of exising diseases.
Accumulating lipid deposits can also form irregular aggregates or bands of adipose tissue that separate myocardial cells. Overeating or experimental obesity studies have found that most of these changes can be incuded with deliberate overeating to achieve excess body fat. An increase in inflammatory cytokines as well as an increase in insulin resistance may be the initiating factors to decrease adiponectin. Its action is to increase insulin resistance; contributing to metabolic syndrome, diabetes, and atherosclerosis. Angiotensin II is the most active form and is a potent vasoconstrictor in the vasculature.


This molecule is found in the innermost layer of the artery; a single cell layer called the endothelium. The genetic defect may be the inability to produce the specific antibody or the inability to produce enough antibody to fight the cancer cells. Natural killer cells, macrophage and neutrophills are increased during times of remission.
Role of adipocyte, free fatty acids, and ectopic fat in pathogenesis of type 2 diabetes mellitus: Peroxisomal proliferative-activated receptor agonists provide a rational theraputic approach. The decrease of adiponectin decreases vascular nitric oxide production which decreases endothelial antiatherogenic function.
Hypertension is the primary outcome, however, inflammation and endothelial proliferation are also associated with RAS substances in overweight and obesity. Elevated PAI-1 upsets the balace between thrombotic (clot formation) and fibronolytic (breakdown of fibrin) systems favoring the formation of thrombi in the artery, accelerating the atherogenic process.
The 3 MET requirement for the walking (above) will be 20% for the 50 kg person, but 42% for the 100 kg person. Endocrine regulation of energy metabolism: Review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin, and resistin. The number of cells are controlled so that the organ remains the proper size; not too big or too small. Department of Health and Human Services, Centers for Disease Control and Prevention, 2008; Mokdad AH, et al.
Normal cells differentiate into specialized functions such as red blood cells or skin cells. Essentially, in cancer, a normal cell becomes a cancer cell, which reproduces in an unchecked manor, eventually taking over the normal cells, but not taking over the normal cell function.



Conventional treatment of type 2 diabetes
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