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

The relationship between obesity, insulin resistance, and hyperinsulinemia is briefly reviewed. The possibility is considered that excess insulin secretion is the cause rather than the result of insulin resistance and obesity. Glucose administration is one of the most frequently studied of those factors known to stimulate insulin secretion. Much less well documented is the fact that meals of equal protein, fat, and carbohydrate content may cause different responses of plasma glucose and insulin. An experiment is reported in which the effects of a high-carbohydrate, high-fiber meal administered to seven healthy young adults were compared with the effects of a meal equally high in carbohydrate but composed largely of glucose in liquid formula form. The high-fiber meal caused an insulin rise less than half that caused by the liquid formula meal although the plasma glucose response to the two meals was not significantly different. The hypothesis is proposed that a high-carbohydrate, fiber-depleted diet, high in simple sugars, by repeatedly stimulating an excessive insulin response, may lead to insulin resistance and obesity in susceptible individuals and may play a role in the common occurrence of obesity in industrialized societies.
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PMID:Dietary fiber, plasma insulin, and obesity. 70 89

Physical training is useful as a therapeutic means to obtain a decrease in body fat. The success in terms of lost fat is dependent on the ability to adhere to the programme, and probably also on regulatory factors associated with the degree of filling of adipose tissue (adipocyte volume). The rate of weight loss is usually slower than with dietary treatment but physical exercise may be more successful and less uncomfortable in the long run as a means to lose weight and prevent regaining it. Physical training is also effective against the metabolic complications associated with obesity such as decreased glucose tolerance, hyperinsulinemia and hypertriglyceridemia and should therefore be a method of choice to prevent or treat adult onset diabetes mellitus and endogenous hypertriglyceridemia in obesity. The feasibility of training in different groups of subjects seems to be dependent on, among other factors, selection of subjects and design of the training programme.
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PMID:Physical training in the treatment of obesity. 71 62

Recent information indicates that the capacity of man to store carbohydrate energy by transformation into fatty acids synthetized de novo is very limited in adipose tissue as well as in liver and intestine. This seems to be in contrast to other species such as the rat where de novo fatty acid synthesis can be induced to a high capacity of glucose removal. This leaves man with a limited capacity to store excess carbohydrate. The remaining possibilities are both the main glycogen stores in liver and in muscle. The latter is by far the largest. The capacity of muscle to assimilate glucose is dependent on its glycogen content that in turn is dependent on previous glycogen depletion to supply energy for muscle contraction. Man might, thus, be uniquely limited in the capacity to dispose of extra carbohydrate in the sedentary state. This might speculatively be thought to be an explanation for a carbohydrate excess syndrome in the sedentary state that may well increase the risk for obesity, hyperinsulinemia, and diabetes mellitus. The logical treatment for such a syndrome then is either a decreased intake of energy as carbohydrate or an increased disposal of carbohydrate energy by exercise. Exercise has, indeed, been shown to have such effects both after physical training programs and, perhaps more pertinent to the question, during a few days after a single exercise bout that has consumed a large amount of muscle glycogen.
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PMID:Carbohydrate storage in man: speculations and some quantitative considerations. 72 37

Animal models with genetic or experimentally produced (lesions of hypothalamus) obesities are numerous and unlikely to ever be reduced to a single pathophysiologic entity. However, obese animals have many similar traits in common. They are all hyperinsulinemic, an abnormality that occurs early in the development of these syndromes and appears to be of prime importance in producing most of the metabolic changes observed both in the early and late phases of the obesity syndromes. In all instances, obesity is an evolutional syndrome in which the early phase is different from the later one. The early phase is principally characterized by increased hepatic very low density lipoprotein (VLDL) output, increased adipose tissue lipogenesis and VLDL uptake, hence, increased fat accretion and fat cell size. These abnormalities are secondary to hyperinsulinemia and can be reversed toward normal by normalizing circulating insulin levels. The late phase is characterized by the continuation of the disorders of the early one plus a superimposed abnormality, the insulin resistance state, that is detectable particularly at the level of adipose and muscle tissues, and eventually brings about hyperglycemia. Insulin resistance is a multifactorial pathological condition that includes at least: (a) a decrease (more or less marked) in insulin binding to target tissues that is responsible for the decrease in tissue sensitivity to the hormone; (b) intracellular defects that are probably responsible for the decreased insulin responsiveness of target tissues. The origin of hyperinsulinemia in animal obesities is still ill-defined. Lesions of the ventromedial hypothalamus (VMH) produce rapid and lasting hyperinsulinemia. Such lesions produce, in addition, increased secretion of insulin and glucagon and changes in pancreatic insulin, glucagon, and somatostatin content in subsequently perfused pancreases. The locus responsible for these effects is not defined and may actually involve a series of interrelated loci. Whatever the latter may be, one of the routes of CNS influence upon endocrine pancreas is the vagus nerve, although a humoral factor has also been claimed. The etiology of hyperinsulinemia in genetically obese animals is unknown. Genetic inheritance could bear primarily upon some hypothalamic or other CNS sites, with secondary alterations in the endocrine pancreas function, or primarily on the islets of Langerhans with possible alteration in the respective function of the A, B, and D cells with resulting excessive insulin secretion.
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PMID:Hyperinsulinemia in obesity syndromes: its metabolic consequences and possible etiology. 72 39

Obesity is the common expression of several diverse interacting genetic, familial and environmental factors. In addition to having hypertrophic fat cells because of inordinate triglyceride accumulation, many patients with childhood-onset obesity and those who are massively obese regardless of age at onset have an excessive number of adipocytes. Several endocrinologic and metabolic abnormalities are associated with obesity. Triglyceride formation in and lipid mobilization from hypertrophic adipocytes are exaggerated. The increased availability of free fatty acids to the liver contributes to the excessive synthesis of triglycerides and very-low-density lipoproteins; thus, hypertriglyceridemia is frequently associated with obesity. Hepatic synthesis and biliary excretion of cholesterol are also increased. Most of the excess cholesterol is stored in fat cells. The plasma concentrations of high-density lipoproteins are decreased. Hyperinsulinemia, which is characteristically found in the obese, leads to a decreased number of insulin receptors in target cells. The relative insulin insensitivity of the obese frequently results in glucose intolerance. The endocrinologic and metabolic abnormalities are correctable by an appropriate program of meal planning and physical activity.
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PMID:Pathophysiologic changes in obesity. 73 17

Colony-bred Wistar-rats develop obesity after long term feeding with a high-fat diet (50% fat, w/w). According to previous investigations a disturbed glucose tolerance after i.v. glucose load could be described for obese rats. Therefore, we measured peripheral IRI-concentrations before and after glucose stimulation in controls and fat-fed rats. In obese animals we observed a basal hyperinsulinemia in the dynamic phase of development of obesity. In controls and fatty rats, no differences in the peripheral insulin response to an i.v. glucose stimulation could be demonstrated, nor did we find indications of an impaired early insulin response in fatty rats. In accordance with the glucose tolerance study, obese rats in the dynamic phase showed lower FFA-levels (fasting state) and a slower decrease of FFA-concentrations after the glucose-induced insulin enhancement. Changing the feeding schedule at 20 weeks of age, e.g. feeding control diets to fatty rats for 4 weeks, reduced basal IRI-concentrations in these animals to control values. Assuming the secondary nature of the basal hyperinsulinemia in obese rats, our present results demonstrate that the observed impairment of glucose tolerance may be related to the peripheral insulin resistance of skeletal muscle and/or hypertrophied adipose tissue.
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PMID:Plasma concentrations of insulin and free fatty acids in dietary-induced obesity of Wistar-rats before and after glucose stimulation. 74 34

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

The present study investigated the effects of subdiaphragmatic vagotomy in rats with ventromedial hypothalamic (VMH) lesions and obesity. Vagotomy or sham-vagotomy was performed two weeks after VMH lesions and rats were observed for 4 more weeks. Complete vagotomy reversed the VMH obesity, lowered serum insulin, lowered basal gastric acid and blocked the secretion of gastric acid after stimulation of the cervical vagus. Pair-feeding of VMH-lesioned rats without vagotomy to the food intake of vagotomized animals also reversed the obesity, lowered serum insulin and lowered basal acid secretion, but it did not prevent the rise in acid after vagal stimulation. These results suggest that subdiaphragmatic vagotomy reversed the obesity of VMH lesioned rats primarily by decreasing food intake. However, there was a positive correlation (r = .70) between the level of serum insulin and basal gastric acid in VMH lesioned rats which remained significant when the effects of food intake were held constant (partial correlation coefficient = 0.449). This supports the possibility that ventromedial hypothalamic injury is followed by enhanced vagal activity and that the vagus may play an important part in the hyperinsulinemia of VMH obesity.
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PMID:The effects of subdiaphragmatic vagotomy in rats with ventromedial hypothalamic obesity. 83 May 33

The deposition of edidymal and perirenal fat, serum insulin levels, and insulin sensitivity of epididymal fat, expressed as the insulin-stimulated production of CO2 from glucose, were determined in Wistar rats fed diets containing either 54% starch or sucrose ad libitum or pair-fed in meals. Regardless of the pattern of feeding, sucrose-fed rats deposited more adipose tissue per 100 g body weight and exhibited less insulin sensitivity than did starch-fed rats. Significant differences in adipose tissue weights were not always accompanied by significant differences in body weights. Meal-fed rats deposited less adipose tissue and showed a greater insulin sensitivity than did ad libitum rats fed the same carbohydrate. However, when changes in feeding pattern negated the difference in adipose weights there was no difference in the insulin sensitivity of the meal-fed and ad libitum-fed rats. Rats consuming the sucrose diet generally exhibited significantly higher fasting serum insulin levels than did rats consuming the starch diet. The serum insulin values tended to be higher in the ad libitum-fpididymal tissue from the meal-fed and starch-fed rats tended to be greater than that of the sucrose-fed or ad libitum-fed rats, respectively, suggesting differences in adipocyte composition. Since obesity, insulin insensitivity, and hyperinsulinism are associated with an impairment of glucose tolerance, the observed metabolic effects of dietary sucrose are considered to be undesirable.
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PMID:Insulin sensitivity and adipose tissue weight of rats fed starch or sucrose diets ad libitum or in meals. 83 76


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