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

During the period from 1974 through 1988, we annually examined approximately 225,000 to 386,400 school children residing in Tokyo for glycosuria to detect juvenile diabetes. If the first test was positive for glucose, glycosuria was confirmed by a second test. In children who gave a positive result in both the first and second tests 0-GTT were performed. All 124 patients were diagnosed as NIDDM according to the criteria of the WHO Report on Diabetes of 1985. The incidence of NIDDM in children in Japan has increased in recent years and from 1984 to 1986 was approximately 3.8 per 100,000 per year. The frequency of NIDDM increases with age up to 14 years. In about 84% of cases, the body weight at diagnosis is more than 20% above the ideal weight and the height is often above average. There is a high frequency in families with a history of diabetes. Diet and exercise therapy in newly diagnosed patients irrespective of the presence or absence of obesity may result in remission, but some cases may require insulin therapy or oral administration of a hypoglycemic drug to obtain a better glycemic control. Children with NIDDM are more likely to be complicated by incipient retinopathy within two years after diagnosis than those with IDDM. Therefore, it is important to keep strict glycemic control to prevent diabetic complications in NIDDM children just as in juvenile onset IDDM.
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PMID:Descriptive epidemiology of non-insulin dependent diabetes mellitus detected by urine glucose screening in school children in Japan. 208 75

Considering pancreatic reserve recognition a more rational basis for starting insulin therapy in NIDDM, during 1988 we studied fasting and post-breakfast plasma C-peptide levels in 31 patients (21 w, 10 m, mean age 48.2 +/- 17.7 yr), referred to our department for insulin therapy evaluation because of primary or secondary failure to other measures. Major features were obesity and chronically uncontrolled illness. Our patients were categorized as follows: group A, considered non responders which included four patients; group B, taken as responders consisting in seven; and a remaining of 20 hyperresponsive patients which formed group C; these with patients of group B, embodied an 87.1% of patients. Among nonresponders there was no any case of total B cell loss of function, and plasma C-peptide activity surpassed through those limits considered for ketoacidosis. We believe that these patients should be eligible candidates for insulin therapy. We failed to found out correlation of plasma C-peptide activity with either age or duration of illness. Our observation supports that fasting plasma C-peptide evaluation would suffice for pancreatic reserve evaluation. We conclude that our patients mainly presented an insulin resistant state associated with obesity thus enhancing the commonplace call for reinforcing nonpharmacologic treatment modalities such as caloric restriction, weight loss and exertion to achieve a better control in NIDDM patients.
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PMID:[C-peptide measurement in patients with type II diabetes mellitus: its possible use in the insulin therapy decision]. 210 99

Obesity is a common problem in Type 2 diabetes mellitus, and reduction of weight in obese diabetic patients will lead to an improvement in glucose tolerance. Despite the importance of weight loss, obese diabetic patients often fail to lose weight with advice on dietary restriction. Frequent visits to see the dietician provide the best chance of successful weight loss, and should be an important part of the management of the overweight patient. If this line of treatment is unsuccessful, then drug therapy may be considered to assist the patient in adhering to the dietary restriction. Over the past decade, drug therapy for weight loss has fallen into disrepute in the wake of the abuse of amphetamines and thyroid hormones by both patients and doctors. For this reason, the only drug commonly used in the diabetic clinic to assist patients to lose weight is metformin because of its putative therapeutic effect on obesity. However, currently available anorectic agents have much less potential for abuse by patients than their predecessors, and new drugs are being developed in this field.
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PMID:Drug treatment of obesity in type 2 diabetes mellitus. 213 66

IGF I and IGF II are insulin-like peptide hormones circulating in blood bound to specific carrier proteins. IGF I mediates many actions of growth hormone--hence its designation as somatomedin C--and it stimulates cell replication, cell differentiation and the synthesis of cellular products (matrix proteins, etc.). Recent investigations in normal human subjects show that pharmacological doses of IGF I increase renal function and have profound metabolic effects that might prove to be useful in the treatment of conditions characterized by relative insulin resistance, such as type 2 diabetes, obesity and hyperlipidemia.
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PMID:[Insulin-like growth factors (IGF I and IGF II) and diabetes]. 215 81

In vivo studies indicate that patients with NIDDM have defects in both insulin secretion and insulin action. The decrease in insulin action is due to both hepatic and extrahepatic insulin resistance. The impairment in glucose uptake is associated with alterations in both oxidative and nonoxidative disposal. Defective glucose transport may limit both of these processes. NIDDM also is associated with increased concentrations and rates of oxidation of plasma free fatty acids. Insulin resistance appears to be familial and in at least some individuals antedates glucose intolerance. In vitro studies indicate that insulin resistance can involve a variety of insulin sensitive tissues including adipocytes, muscle and liver. While most studies note that insulin binding and insulin receptor kinase activity are decreased in insulin sensitive tissues in obese patients with NIDDM, further delineation of the contribution of obesity and diabetes is required. Alterations in glucose transporter number and function likely account at least in part for impaired glucose transport. The cause of the alterations in other insulin responsive pathways and the role of an abnormal metabolic milieu versus intrinsic cellular defects remain to be established.
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PMID:Insulin resistance in type II diabetes mellitus. 216 26

Young female obese (cp/cp) and lean littermates (?/+) of the recently developed congenic strain, SHR/NIH-corpulent (SHR/N-cp), were fed for 6.5 months isocaloric diets containing 54 percent carbohydrate as either sucrose or starch. Glycemic, lipidemic and renal parameters were determined after 1, 3 and 6 months. Systolic blood pressure and plasma corticosterone levels were determined after 3 months. After 6.5 months rats were killed for histological examination. Obese rats were hyperglycemic following an oral glucose challenge (1 hour response greater than 11.1 mmol/l) (200 mg/dl), hyperinsulinemic, hypertriglyceridemic, and developed proteinuria and mild hypertension. Feeding sucrose, as compared to starch, further increased serum glucose, insulin and triglyceride levels and urinary protein excretion in obese rats and serum triglyceride levels in lean rats. An amelioration of glucose intolerance was observed in sucrose-fed obese rats by 6 months. In contrast to serum insulin levels, serum triglyceride levels increased with age in obese rats. Obese rats exhibited hypertrophy of the kidney and adrenal cortex with abnormal histology. The study demonstrates that obese female SHR/N-cp rats exhibit some of the metabolic and histopathological changes associated with NIDDM in humans and that feeding sucrose, as the source of dietary carbohydrate, further magnifies the expression of diabetes in this model.
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PMID:Influence of genetic obesity, dietary carbohydrate and age on parameters of glucose tolerance and kidney and adrenal gland histology in female SHR/N-corpulent rats. 217 55

We tested the hypothesis that insulin resistance, rather than high insulin level, is associated with lipid and lipoprotein changes favoring atherosclerosis independently of the glucose tolerance status. To this aim, 50 subjects with normal glucose tolerance, 28 subjects with impaired glucose tolerance, and 54 subjects with noninsulin-dependent diabetes (NIDDM) were studied. Subjects with low glucose disposal rate (GDR) or a high degree of insulin resistance as measured by the euglycemic hyperinsulinemic clamp technique had lower high density lipoprotein (HDL) cholesterol and higher total and very low density lipoprotein (VLDL) triglycerides than did subjects with high GDR (highest GDR tertile). These associations were independent of fasting insulin level and other confounding factors. In stepwise multiple linear regression analysis, GDR was the most important single variable associated with HDL cholesterol and VLDL triglyceride level independently of age, obesity, distribution of obesity (waist/hip ratio), 2-hour glucose level, and free fatty acid concentration. We conclude: 1) insulin resistance measured by the euglycemic clamp technique is associated with adverse lipid and lipoprotein changes favoring atherosclerosis not only in nondiabetic subjects (as shown in previous studies) but also in impaired glucose tolerance and NIDDM subjects; 2) the association of high insulin level with adverse lipid and lipoprotein changes indirectly reflects the association of insulin resistance with lipid and lipoprotein levels; and 3) HDL cholesterol and VLDL triglycerides are independently associated with insulin-mediated glucose uptake, which may indicate that these lipoproteins have separate sites of interaction with insulin action.
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PMID:Insulin resistance is associated with lipid and lipoprotein abnormalities in subjects with varying degrees of glucose tolerance. 218 Mar 96

The author discusses the very low calorie diet and its physiopathological effects, in the treatment of NIDDM with obesity. In the latter condition the very low calorie diet can be utilized in order to obtain the desired body weight decrease, and consequently to improve glucose tolerance; however, this goal can only be reached by including in the diet sufficient amounts of carbohydrates, and by following some identified parameters of the treated patient.
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PMID:[Semifasting and type II diabetes mellitus]. 219 12

Several epidemiological studies have reported that the regional distribution of body fat is a significant and independent risk factor for cardiovascular disease (CVD) and related mortality. Although these associations are well established, the causal mechanisms are not fully understood. Numerous studies have, however, shown that specific topographic features of adipose tissue are associated with metabolic complications that are considered as risk factors for CVD such as insulin resistance, hyperinsulinemia, glucose intolerance and type II diabetes mellitus, hypertension, and changes in the concentration of plasma lipids and lipoproteins. The present article summarizes the evidence on the metabolic correlates of body fat distribution. Potential mechanisms for the association between body fat distribution, metabolic complications, and CVD are reviewed, with an emphasis on plasma lipoprotein levels and plasma lipid transport. From the evidence available, it seems likely that subjects with visceral obesity represent the subgroup of obese individuals with the highest risk for CVD. Although body fat distribution is now considered as a more significant risk factor for CVD and related death rate than obesity per se, further research is clearly needed to identify the determinants of body fat distribution and the causal mechanisms involved in the metabolic alterations. It appears certain, however, that an altered plasma lipid transport is a significant component of the relation between body fat distribution and CVD.
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PMID:Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. 219 40

This report presents an overview of the prevalence, characteristics, morbidity, mortality, and risk factors for noninsulin-dependent diabetes (NIDDM) in Blacks and Whites in the United States. Data are drawn primarily from national surveys, but the report also includes the few clinical studies that have differentiated the two races. NIDDM constitutes 90-95% of all diabetes in the United States and is more prevalent in Black Americans than in Whites. Diabetes prevalence increases with age for both races and reaches 26% among Blacks aged 65-74 years compared with 18% among Whites. Rates of diabetes among persons aged 20-74 years are 30% higher in White women, 70% higher in Black men, and 100% higher in Black women, compared with White men. Approximately half of diabetes is undiagnosed in both races. White and Black diabetics are similar with regard to age, duration of diabetes, and diabetes therapies, although Blacks of both sexes are more obese than their White counterparts. Rates of vision loss, amputations, and renal disease are 1.5-4 times higher in Blacks than in Whites, although prevalence of hypertension is about equal in the two races. Blacks and Whites see the same physician specialists for their diabetes, but Whites have approximately 40% more visits to office-based physicians each year. Diabetes-specific mortality has declined significantly in the past decade and may now be lower in Black than in White diabetics. Risk factors for diabetes, including age, sex, obesity, and family history of diabetes, all operate within both race groups and probably interact with each other. The effect of gender and family history on rates of diabetes is similar in Blacks and Whites. Blacks have higher rates of diabetes at each obesity level, indicating that obesity alone cannot explain the differential in prevalence between the races. Impaired glucose tolerance (IGT), a strong risk factor for development of diabetes, increases with age in all race/sex groups except for Black women older than 54 years in whom rates of IGT, decline, possibly because of conversion of IGT to diabetes.
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PMID:Noninsulin-dependent diabetes mellitus in black and white Americans. 219 51


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