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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A spontaneously diabetic rat with polyuria, polydipsia, and mild obesity was discovered in 1984 in an outbred colony of Long-Evans rats, which had been purchased from Charles River Canada (St. Constant, Quebec, Canada) in 1982. A strain of rats developed from this rat by selective breeding has since been maintained at the Tokushima Research Institute (Otsuka Pharmaceutical, Tokushima, Japan) and named OLETF. The characteristic features of OLETF rats are 1) late onset of hyperglycemia (after 18 wk of age); 2) a chronic course of disease; 3) mild obesity; 4) inheritance by males; 5) hyperplastic foci of pancreatic islets; and 6) renal complication (nodular lesions). Histologically, the changes of pancreatic islets can be classified into three stages: 1) an early stage (6-20 wk of age) of cellular infiltration and degeneration; 2) a hyperplastic stage (20-40 wk of age); and 3) a final stage (at > 40 wk of age). These clinical and pathological features of disease in OLETF rats resemble those of human NIDDM.
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PMID:Spontaneous long-term hyperglycemic rat with diabetic complications. Otsuka Long-Evans Tokushima Fatty (OLETF) strain. 139 18

Amylin, also called islet amyloid polypeptide (IAPP), or diabetes-associated peptide (DAP) is a recently discovered 37 amino acid polypeptide which has been shown to be co-secreted with insulin from the pancreatic beta-cell. The peptide turned out to be the major constituent of pancreatic amyloid deposits which are frequently found in the pancreas of type II diabetic patients. Therefore, a role for amylin in the aetiology of type II diabetes was hypothesized. To investigate this possibility, several studies have been performed to elucidate whether amylin is able to impair insulin secretion and action, two characteristic features of type II diabetes mellitus. These studies suggest that it is unlikely that amylin has a direct inhibitory effect on insulin secretion. Amyloid deposits, however, which are derived from the in situ polymerization and precipitation of amylin, may impair beta-cell function during type II diabetes by damaging and covering beta-cells. Furthermore, it has been shown that amylin has the potential to antagonize the action of insulin on glucose metabolism by increasing hepatic glucose production and by decreasing muscle, but not adipocyte glucose uptake. For these reasons, it has been suggested that amylin might be involved in the pathophysiology of type II diabetes and obesity, disease states which are characterized by abnormal beta-cell function and insulin resistance. In addition, amylin was shown to induce hypocalcaemia by inhibiting osteoclast-mediated bone resorption in a calcitonin-like manner. Therefore, amylin is likely to be involved in both the modulation of glucose and calcium metabolism.
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PMID:Biological action of pancreatic amylin: relationship with glucose metabolism, diabetes, obesity and calcium metabolism. 140 45

Information concerning cardiovascular disease risk factors in Native American children is limited. In adult Native American populations, cardiovascular disease risk factors of non-insulin dependent diabetes mellitus, obesity, and cigarette smoking are prevalent, and recent reports indicate mortality caused by cardiovascular disease has dramatically increased. In a screening program at the Onondaga Nation School, six cardiovascular disease risk factors were evaluated. Of 95 school children, 55 representing 39 interrelated families, participated. Family histories were positive for diabetes mellitus in 72%, for cardiovascular disease in 54%, and for passive smoking in 90% of families. Physical examinations of the children revealed obesity (weight/height greater than 90th percentile) in 42% and hypertension (systolic or diastolic blood pressure/height greater than 95th percentile) in 22%. Fingerstick cholesterol levels (Reflotron system) were greater than 170 mg/dL in 25%. Overall, 85% of participants had three or more risk factors for cardiovascular disease. The study results indicate that Onondaga Native American children are at significant risk for cardiovascular disease; programs for identification and modification of cardiovascular disease risk factors are urgently needed.
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PMID:Cardiovascular risk factors in Native American children. 140 96

Twenty-five middle-aged subjects with impaired glucose tolerance (IGT) were analysed 5 years later, showing normal glucose tolerance in 28% and persistent glucose deterioration in 72%. Body mass index (strongly) and 2-h glucose levels were clinically useful predictors, in the newly detected IGT-subjects, of persistent glucose deterioration (IGT or NIDDM) 5 years later. The frequency of hypertension was 36% in the newly-detected IGT subjects. Five years later this frequency increased to 54% in the persistently hyperglycaemic group, and decreased to none in the normalized group. Predictors of hypertension at the follow-up were baseline blood pressure and parts of the hyperinsulinaemic syndrome, such as serum triglyceride at baseline, BMI and 2-h glucose at the follow-up. Microalbuminuria (greater than 20 mg day-1) was not found at the 5-years follow-up, either if the subjects then had NIDDM, IGT or normal glucose tolerance. ECG abnormalities (ST segment and T wave changes) were two-fold more prevalent in the group with IGT or NIDDM than in the normalized group at the follow-up. Predictors were baseline BMI and incremental BMI. In conclusion, obesity and high 2-h glucose in newly-detected IGT-subjects seemed to predict the persistence of IGT 5 years later. Hypertension, but not microalbuminuria, was frequent when glucose deterioration persisted.
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PMID:What causes impaired glucose tolerance to deteriorate or normalize? 141 Dec 61

The entry of glucose into muscle cells is achieved primarily via a carrier-mediated system consisting of protein transport molecules. GLUT-1 transporter isoform is normally found in the sarcolemmal (SL) membrane and is thought to be involved in glucose transport under basal conditions. With insulin stimulation, glucose transport is accelerated by translocating GLUT-4 transporters from an intracellular pool out to the T-tubule and SL membranes. Activation of transporters to increase the turnover number may also be involved, but the evidence is far from conclusive. When insulin binds to its receptor, it autophosphorylates tyrosine and serine residues on the beta-subunit of the receptor. The tyrosine residues are thought to activate tyrosine kinases, which in turn phosphorylate/activate as yet unknown second messengers. Insulin receptor antibodies, however, have been reported to increase glucose transport without increasing kinase activity. Insulin resistance in skeletal muscle is a major characteristic of obesity and diabetes mellitus, especially NIDDM. A decrease in the number of insulin receptors and the ability of insulin to activate receptor tyrosine kinase has been documented in muscle from NIDDM patients. Most studies report no change in the intracellular pool of GLUT-4 transporters available for translocation to the SL. Both the quality and quantity of food consumed can regulate insulin sensitivity. A high-fat, refined sugar diet, similar to the typical U.S. diet, causes insulin resistance when compared with a low-fat, complex-carbohydrate diet. On the other hand, exercise increases insulin sensitivity. After an acute bout of exercise, glucose transport in muscle increases to the same level as with maximum insulin stimulation. Although the number of GLUT-4 transporters in the sarcolemma increases with exercise, neither insulin or its receptor is involved. After an initial acute phase, which may involve calcium as the activator, a secondary phase of increased insulin sensitivity can last for up to a day after exercise. The mechanism responsible for the increased insulin sensitivity with exercise is unknown. Regular exercise training also increases insulin sensitivity, which can be documented several days after the final bout of exercise, and again the mechanism is unknown. An increase in the muscle content of GLUT-4 transporters with training has recently been reported. Even though significant progress has been made in the past few years in understanding glucose transport in skeletal muscle, the mechanisms involved in regulating transport are far from being understood.
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PMID:Regulation of glucose transport in skeletal muscle. 142 62

Structural changes in both biliary tract and pancreas have been assessed with endoscopic retrograde cholangiopancreatography in 100 diabetic patients divided into subgroups depending on the type of diabetes mellitus, i.e. type I, type II and III-pancreatic. Control group included 100 randomly selected patients without diabetes mellitus in whom endoscopic retrograde cholangiopancreatography has been performed for various indications. Structural changes in the biliary tract and pancreas have been more frequent in diabetic patients than in the control group (47 and 75% vs 32 and 30%, respectively). Cholelithiasis has been noted in 27.8% of patients with type II diabetes mellitus and in 11.3% of patients with type I diabetes mellitus; obesity has been found in 57 and 12% of patients, respectively. Other biliary tract disorders, mainly in the form of segmental stenosis or dilatation of the common bile duct, have been more frequent in patients with type II diabetes mellitus. Pancreatic disorders, assessed with the aid of Cambridge classification, have been noted in all patients with pancreatic diabetes and in 80.7% of patients with diabetes mellitus type I. Incidence of so-called doubtful and mild disorders has been more frequent (22.2 and 24.1%, respectively) in patients with diabetes mellitus type II whereas "moderate" and "severe" disorders have been significantly less frequent (7.4 and 1.9% of patients). The results indicate, that endoscopic retrograde cholangiopancreatography is useful in the assessment of bile ducts structure and pancreatic exocrine activity in diabetic patients in whom disorders are more frequent.
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PMID:[Anatomic changes in the biliary tract and pancreas in patients with diabetes mellitus diagnosed by endoscopic retrograde cholangiopancreatography]. 143 89

The relationship between obesity and type II diabetes mellitus is well established and a majority of type II diabetic individuals are classified as obese. The pathogenesis of type II diabetes mellitus is not fully understood; however, multiple organ systems are involved, including abnormalities of insulin secretion, peripheral insulin resistance and hepatic insulin resistance. The goal of the treatment for the obese diabetic is to normalise these alterations and achieve normoglycaemia. Traditionally, the initial therapy, aiming to accomplish weight reduction, is diet and exercise. In obese type II diabetic patients, the whole body insulin-dose response curve is markedly depressed. A single exercise session improves and partially normalises both insulin responsiveness and sensitivity for glucose utilisation. Furthermore, a single bout of physical activity often results in decreased plasma glucose levels, which persists into the postoperative period. Type II diabetes patients participating in regular exercise programmes can potentially improve their metabolic control. An improved glucose control in both lean and obese type II diabetic patients under the age of 55 years has been demonstrated by improved HbA1C levels and glucose tolerance tests following physical training programmes. The effect of regular exercise on the metabolic control in these younger patients does not appear to be correlated with weight reduction. For most type II diabetic men over 55 years of age, physical training is not a feasible form of therapy because of other interfering diseases which may complicate or severely hinder all physical training apart from very low intensity exercise programmes. Lean, older, type II diabetic patients who have been able to exercise for 10 weeks or up to 2 years demonstrate no change in HbA1C levels, glucose tolerance or bodyweight. Thus, there is a clear difference in metabolic response to regular exercise between younger and older type II diabetic patients. The younger patient appears to be more inclined to respond to physical training with improvements in the metabolic control. The reason for this apparent difference is not clear, but possible explanations may include differences in training intensity, the presence or degree of complicating diseases, pretraining level of metabolic control or bodyweight. Type II diabetics are predisposed to cardiovascular disease and are characterised by hyperlipidaemia. In obese type II diabetic individuals, physical training improves the blood lipid profile as measured by decreased levels of triglycerides and total cholesterol. In young, overweight diabetics, improved lipid profiles can be achieved despite no change in bodyweight, while no apparent effects are reported for lean patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exercise training in obese diabetic patients. Special considerations. 143 93

The authors summarize the principles of the therapeutic approach to the 5H syndrome [1. hyperinsulinism, 2. hyperglycaemia (NIDDM), 3. hyperlipoproteinaemia (obesity), 4. hypertension, 5. hirsutism], in particular its two components, i.e. NIDDM and arterial hypertension. The authors found that early treatment of hyperinsulinism, e.g. already in the stage of impaired glucose tolerance or NIDDM with oral antidiabetics, their disproportionate increase with regard to the blood sugar level and glycosylated haemoglobin without making "hygienic" provisions (radical weight reduction; increased physical activity to the maximum possible individual level; energy restricted diet in particular as regards carbohydrates and fat) does not prevent progression of the components of the 5H syndrome to the clinical stage. In treatment of arterial hypertension associated with 5H syndrome non-selective beta-blockers and thiazide diuretics are unsuitable because they worsen the HPLP and enhance insulin resistance. Suitable preparations are combinations of ACE-inhibitors, calcium antagonists, selective beta-blockers in particular with ISA and beta-blockers with a partial selective sympathomimetic activity (devalol and celiprolol). Hygienic provisions must be started in childhood, or when hyperinsulinism is detected.
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PMID:[How should we implement the basic principles of treatment of type 2 diabetes mellitus from the aspect of the hormono-metabolic syndrome X (5H)?]. 145 53

The clinical linkage of hypertensive cardiovascular disease, left ventricular hypertrophy, and accelerated atherosclerosis with a spectrum of metabolic disturbances including peripheral insulin resistance, hyperinsulinemia, obesity, and frank non-insulin dependent diabetes mellitus, has been increasingly appreciated. However, the underlying biologic basis mediating this clinical association remains unclear. Nuclear magnetic resonance techniques have been used to measure various intracellular ion species in human erythrocytes and have found that common, shared intracellular abnormalities of cytosolic free calcium, free magnesium, and pH occur in each of these clinical syndromes. Specifically, essential hypertension is characterized by higher fasting free cytosolic calcium concentrations and reciprocally lower intracellular free magnesium and pH levels compared with those of normotensive control subjects. Furthermore, for all subjects, free calcium and free magnesium levels were closely related both to the left ventricular mass and to the degree of insulin resistance present. Moreover, these same intracellular ionic lesions were found in normotensive obese and/or non-insulin diabetic individuals. Last, evidence has recently been provided that the cardiovascular consequences of increased dietary sugar and salt intake may well be determined by their concurrent influence on cellular ion metabolism. These data led to a hypothesis for a central role for altered cellular ion homeostasis in mediating the clinical linkage of cardiovascular and metabolic disease. According to this ionic hypothesis, essential hypertension, non-insulin dependent diabetes, and their frequently associated features of obesity, left ventricular hypertrophy, and accelerated atherosclerosis all derive from and reflect different clinical manifestations of the same underlying cellular lesion, characterized at least in part by elevated cytosolic free calcium and suppressed free magnesium levels.
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PMID:Cellular ions in hypertension, insulin resistance, obesity, and diabetes: a unifying theme. 145 64

Non-insulin-dependent diabetes mellitus is epidemic among African-American women in the United States; reports of its prevalence among African Americans range from 50% to 60% higher than among whites. African Americans also incur higher rates of diabetes-related complications such as blindness, end-stage renal disease, and amputations. Data indicate that non-insulin-dependent diabetes among African Americans is associated with lower socioeconomic status and with obesity. Because obesity has been hypothesized as contributing to the growing numbers of non-insulin-dependent diabetics among African-American women, new strategies are urgently needed to promote weight loss in this population. Community organization can broaden health education and facilitate behavior change toward development of life- and self-mastery skills. Specific strategies of this approach include (1) integrating community values into health messages, (2) facilitating neighborhood "ownership" and decision-making, (3) utilizing existing formal and informal networks, and (4) empowering individuals and community. Community organization may be a promising strategy among low-income minority communities to reduce the risk of non-insulin-dependent diabetes by promoting changes in dietary patterns, because it ensures that the health messages and programs that emerge will be consistent with existing sociocultural norms and beliefs.
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PMID:Community organization to reduce the risk of non-insulin-dependent diabetes among low-income African-American women. 146 55


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