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

Spontaneous hyperglycemia, hyperinsulinemia and obesity are common features for at least one period of the lifetime in some strains of mice. Both genetic and environmental factors are involved in the pathogenesis of the diabetes-like syndrome, making these strains excellent models for studies in both obesity and diabetes-like states. The metabolic peculiarities can be due to a dominant gene, as for the yellow obese, or a single recessive gene, as in the obese and the diabetes mouse; or they can be of polygenic origin, as for the KK and the NZO mouse. However, the severity of the metabolic disorder is due to the interaction of the mutant genes iwth modifiers in the bat genes themselves. Studies on the pathophysiology and biochemistry of these animals have revealed interstrain differences, different patterns of development of the metabolic disorder, and different degrees of severity of the diabetes-like syndrome. Although the primary causes of the syndrome remain unclear in some strains, an involvement of hypothalamic feeding centers has been implicated.
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PMID:Laboratory animals exhibiting obesity and diabetes syndromes. 83 44

In 158 obese children, aged from three months to 15 years, blood glucose, immunoreactive insulin, and free fatty acid levels were measured during a standard oral glucose tolerance test carried out prior to treatment. The results were analyzed for the total sample as well as for three age groups: 0-5 years, 6-10 years, and 11-15 years and compared with those of 70 normal-weight children matched for age and sex. Glucose tolerance is normal in the obese children. It is different from the controls only two hours after glucose loading, when a slight but significant elevation is found. The glucose levels at one and two hours are significantly higher in the obese children of group III than in the younger ones. Fasting F.F.A. levels are similar in normal and obese children, but the F.F.A. decrease following glucose absorption is significantly diminished in the obese. The F.F.A. levels of the youngest obese are significantly higher than those of the older ones. A constant and important hyperinsulinism, fasting and postabsorptive, is demonstrated in obese children of all ages, even before five years and at the beginning of obesity. Age- and sex-related differences in insulin secretion are much more marked in the obese than in normal children. The degree of hyperinsulinemia is related to the degree of obesity, but not to its duration. The results suggest that hyperinsulinism is associated with obesity from its onset rather than being a long-term consequence of overweight. However, the origin of hyperinsulinism in obesity and the mechanism of insulin resistance still remain obscure.
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PMID:Blood glucose, insulin, and free fatty acid levels during oral glucose tolerance tests in 158 obese children. 83 67

A new automated potentiometric method for the determination of colipase was developed, taking advantage of the reactivation of purified lipase, in the presence of bile salt and at pH 6.5. High-fat and high-starch diets induced an opposite regulation of lipase and amylase in the rat pancreas. At the same time, the level of colipase was not influenced by nutrition. During fasting and in alloxan diabetes, the specific activity of lipase almost doubled, that of amylase decreased sharply, and colipase was not affected in the rat pancreas. In obese-hyperglycemic mice, suffering from obesity, hyperinsulinism, and moderate diabetes, there was also no regulation of pancreatic colipase. Thus, at variance with a number of hydrolases, there was no dietary or hormonal adaptation of colipase. However, this was probably without any bearing on intraluminal lipolysis. Indeed, comparison of lipase and colipase activities in pancreas and in small intestine suggests that colipase concentration is not a limiting factor of intraluminal lipolysis. The molecular mechanism of this assumption is discussed on the basis of in vitro studies.
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PMID:Lack of adaptation of pancreatic colipase in rats and mice. 84 20

With the purpose of investigating the pathogenesis of obesity and hyperinsulinemia in rats with hypothalamic lesions (HTL), HTL were made in vagotomized rats, and the development of obesity was serially followed up to 15 weeks as well as the changes of plasma triglyceride and immunoreactive insulin (IRI) levels. Even in vagotomized rats, obesity developed after HTL and plasma triglyceride and IRI levels increased significantly. However, obesity was slightly less in grade and occurred later as compared with sham-vagotomy-HTL rats. Plasma IRI levels in vagotomized rats significantly correlated with the body weight, Lee's index, the weight of adipose tissue and plasma triglyceride level. Similar results were also obtained in rats with HTL which were pair-fed following vagotomy. These results suggest that the hyperinsulinemia in obese rats with HTL may be involved not only by hypersecretion of insulin mediated by hypothalamo-vagal nerve system but also by some insulin-antagonistic factors such as increases of adipose tissues and plasma lipids.
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PMID:Effect of vagotomy on hyperinsulinemia in obese rats with hypothalamic lesions. 91 35

The response of plasma insulin concentration to an oral glucose tolerance test (OGTT) and to the maximum stimulatory effect obtained with administration of glucose, glucagon and tolbutamide was studied in 24 siblings of diabetic children and in ten obese children. Five siblings of patients with diabetes sound to have chemical diabetes had hyperinsulinism during the OGTT. Serum insulin concentrations during the maximum stimulation of the beta cells in the children with chemical diabetes, although diminished at 15 minutes, were considered not significantly different from controls. Obese children had hyperinsulinism during the OGTT and the maximum stimulation of the beta cell. The data suggest that hyperinsulinism may precede or accompany carbohydrate intolerance in siblings of diabetic children.
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PMID:Maximum stimulation of insulin secretion in children with chemical diabetes and obesity. 94 38

Eighteen obese inpatients with insulin resistance revealed by i.v. insulin test and expressed in various grades of hyperinsulinemia and hyperglycemia were examined for plasma lipid levels. A significant positive correlation was found to be present between the plasma triglyceride (TG) level and the insulin response to glucose load. A stepwise multiple regression analysis revealed that the insulin secretory response, the plasma cholesterol level and the relative body weight contributed to the level of plasma TG. No difference was found in the grades of insulin resistance between patients with and without elevated TG. The ratio of sum of plasma insulin values to that of blood glucose values during glucose tolerance test was markedly increased in patients with elevated TG. The patients with relatively blunted insulin response and impaired glucose tolerance curves showed only slight slight hypertriglyceridemia. Endogenous hypertriglyceridemia in obesity seems to be more closely correlated with plasma insulin level, and therefore, with insulin action rather than insulin resistance.
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PMID:Relationship between insulin secretory function and endogenous hypertriglyceridemia in obese humans with insulin resistance. 96 Jan 1

To evaluate the role of insulin in familial hypertriglyceridemia, 34 relatives of the pedigrees of 3 index cases of endogenous hypertriglyceridemia and hepatic steatosis as well as 9 spouses were examined for plasma lipids and responses of blood glucose and plasma insulin during oral glucose tolerance tests. The combined disorders of hypertriglyceridemia and hyperinsulinemia plus glucose intolerance--insulin resistance--were most commonly found among the relatives, which were often accompanied by an impaired liver function. Some relatives showed hyperinsulinemia without hypertriglyceridemia. Obesity was frequent, but its incidence was similar to the controls. Thus, the observed form of familial hypertriglyceridemia was apparently coupled with insulin resistance; and hyperinsulinemia, or insulin resistance by itself, might be a basic genetical trait in this form of lipid disorder.
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PMID:Evidence for a familial form of hypertriglyceridemia as disorders coupled with insulin resistance. 96 Jan 7

Long term feeding of a sucrose rich diet to rats is accompanied by a decreased glucose assimilation rate, despite high plasma insulin levels. Hyperinsulinism is at least partially based on a relative obesity, with increased amounts of abdominal- and retroperitoneal fat tissue, but unchanged total body weight compared to starch fed controls. The secretory pattern of insulin release was studied following glucose, arginine, fructose and sulfonylurea administration in the isolated perfused pancreas of sucrose and isocaloric starch fed rats. In addition, isolated islets of Langerhans were used to demonstrate the effects of glucose on insulin secretion and the incorporation of H-3 leucine into the proinsulin and insulin fraction of islet proteins. Following 11 mM glucose, the dynamics of insulin release in the isolated perfused pancreas of sucrose fed rats is characterized by a markedly elevated, late plateau-like response, usually seen only at higher glucose concentrations. Hyperinsulinism, as compared to starch fed controls, can also be demonstrated following arginine and the sulfonylurea HB-419, whereas fructose has no effect in the presence of low glucose concentrations. During incubation of the pancreatic islets, the hyperinsulinism in sucrose-, compared to starch fed rats, is more pronounced at 11 mM glucose than at 5.5 mM glucose. The incorporation of H-3 leucine into the proinsulin-insulin fraction of islet proteins in sucrose compared to starch fed rats, however, is significantly greater with glucose 5.5 mM than at high glucose level. In sucrose fed rats, secretion and biosynthesis of insulin thus appear to be elevated but closely linked only at physiological glucose concentration.
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PMID:Insulin secretion and biosynthesis in sucrose fed rats. 97 34

Previous reports agree that estrogen and estrogen-containing contraceptives increase serum triglyceride levels of normal women, but disagree on their effect on serum cholesterol levels. Since obesity is often accompanied by hyperinsulinemia and since hyperinsulinemia may participate in production of hypertriglyceridemia, we investigated the effect of oral contraceptives on the serum lipids of obese women. Serum triglycerides and cholesterol were measured before and after 3 months administration of the contraceptives. The mean triglyceride level increased 23% in the obese and 21% in the normal women. The mean cholesterol level increased 6% (P less than 0.05) in the obese and did not change in the normal women. The increase in cholesterol occurred mostly in those with initial levels less than 225 mg/100 ml; in those with initial levels above 250 mg/100 ml the level usually decreased with treatment. The serum lipid changes were not related to the serum insulin levels.
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PMID:Serum lipid changes during contraceptive administration in obese women: relation to serum insulin levels. 97 25

The development of obesity, hyperglycemia, and hyperinsulinemia, was examined in obese-hyperglycemic (ob/ob) mice, their lean littermates, and homozygous lean mice (+/+) between 17 days and 8 wk of age. By 4 wk of age ob/ob mice displayed many of the metabolic characteristics that are typical of the syndrome in adult animals, including elevated systemic insulin and glucose levels, increased body weight, obesity, reduced skeletal growth, and in vivo evidence of insulin resistance. In addition, 4-wk-old lean littermates of obese mice had greater body weights, increased per cent carcass lipid, and higher insulin levels than did +/+ mice of the same age that were raised under identical conditions. At 17 or 21 days of age ob/ob mice, defined by either (1) elevated carcass fat content when compared to littermates at time of killing or (2) by phenotypic expression of obesity at 6 wk of age, exhibited moderate hyperinsulinemia, hypoglycemia, reduced skeletal growth, and "obesity", as expressed by the Lee index. The present results indicate that altered pancreatic beta-cell function, obesity, and abnormalities of somatic growth all precede the onset of hyperglycemia and insulin "resistance" in ob/ob mice. Furthermore, the occurrence of these characteristics before 17 days of age suggests that the transition to laboratory diet is not essential for the expression of the ob mutation. The present data also support recent studies that have described a small but reliable effect of the ob gene on the metabolism of heterozygous lean mice.
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PMID:The development of obesity, hyperinsulinemia, and hyperglycemia in ob/ob mice. 99 38


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