Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three obese women were admitted as inpatients to a metabolic ward and had an average intake of 3.35 MJ (800 kcal) daily for three weeks. Fat biopsies were taken at three subcutaneous sites and average fat cell mass (CM) and apparent fat cell number (FCN) were calculated. There was no significant correlation between adipose tissue cellularity (CM or FCN) and total weight loss or resting metabolic rate, provided due allowances were made for the severity of obesity in each case. Neither was there any significant correlation between short-term weight loss and the age of onset of obesity. Resting metabolic rate, and not adipose tissue cellularity or age of onset of obesity, is a better indicator of short-term weight loss under controlled inpatient conditions.
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PMID:Does adipose tissue cellularity or the age of onset of obesity influence the response to short-term inpatient treatment of obese women? 15 80

The role of substrate cycles in metabolic control was first indicated over ten years ago, but the recent interest in such cycles has developed from the direct demonstration by isotopic techniques of their existence in various tissues. I propose that substrate cycles form part of a logical series of biochemical mechanisms that exist to increase the sensitivity of non-equilibrium reactions to changes in concentrations of metabolic regulators. The possible importance of such cycles for provision of precise metabolic regulation in the tissues of the normal subject and the trained athlete is proposed. Furthermore, cycling may provide a mechanism by which hormones can change the magnitude of response in a tissue to a given metabolic signal, without interfering in the biochemistry of the basic control mechanism. It is, however, possible to extend the role of cycling to heat generation and thus to controlled energy loss by an organism. Heat generation by substrate cycles may be important as an acute mechanism for maintaining the body temperature in man in response to a sudden decrease in the environmental temperature; alcoholic hypothermia would be explained by inhibition of substrate cycling in the liver, and accidental hypothermia in the elderly could be explained by decreased capacity of substrate cycles with age. If heat generated by the cycles is rapidly lost to the environment, the expenditure of energy to maintain this heat loss could explain, in part, the physiological phenomena of the thermic response to food and the oxygen debt which is always observed after exercise. Finally, the energy expended in these ways could be part of a general biochemical mechanism for maintenance of the correct body weight; a decrease in the capacity of substrate cycles might be one factor involved in the development of obesity.
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PMID:Substrate cycles: their metabolic, energetic and thermic consequences in man. 15 56

Carbohydrate metabolism was studied in eight patients with Down's syndrome, aged 8 to 18 years. Diabetic glucose tolerance was observed in only one patient with obesity. This impaired glucose tolerance was improved with the weight reduction due to diet restriction. The flat glucose tolerance curves with low peak values were also observed in the other two patients. In the remaining five patients, normal glucose tolerance was obtained. Insulin response and free fatty acid levels during oral glucose load were not characteristic except for the diabetic patient with obesity. The sera of Down's syndrome showed normal binding capacity for insulin. These results suggest that obesity might partly participate in the impaired glucose tolerance in Down's syndrome.
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PMID:Carbohydrate metabolism in Down's syndrome. 16 Jun 33

Plasma levels of gonadotropins, PRL, T4, and adrenal and gonadal steroids were measured in two groups of 7- to 9-yr-old and 10- to 11-yr-old obese prepubertal girls, and were compared to those found in groups of nonobese girls of the same age. The data found in normal weight subjects confirm the data reported in the literature, showing a significant rise between the 7- to 9- and 10- to 11-yr groups, of FSH, pregnenolone, dehydroepiandrosterone, testosterone, and estradiol plasma levels, while LH, PRL, T4, cortisol, progesterone, 17-hydroxyprogesterone (17P), and androstenedione remained constant. In the obese subjects, pregnenolone and dehydroepiandrosterone levels are notably higher than in the normal girls, in the same range as those found in adult women; furthermore, they show no rise between the two age groups. The obese prepubertal groups had significantly higher progesterone, androstenedione, and PRL levels in comparison with those observed in girls of normal weight, but 17-hydroxyprogesterone, cortisol, testosterone, LH, and T4 were similar in both groups. Estradiol levels were markedly depressed in the obese girls; FSH levels were higher in the younger girls than in normal subjects. These data indicate that in prepubertal obesity, maturation of adrenal gland function (chiefly the delta 5 pathway), is notably enhanced, whereas gonadal secretion of estradiol is impaired in the presence of high levels of FSH and PRL.
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PMID:Plasma levels of gonadotropins, prolactin, thyroxine, and adrenal and gonadal steroids in obese prepubertal girls. 16 19

Glycerokinase activity in isolated fat cells was elevated in both Ob/Ob and Db/Db mice in comparison to their lean controls and this elevation was associated with obesity, hyperinsulinemia and hyperglycemia. In the other forms of acquired and genetic obesity in the rats and mice studied (also associated with hyperinsulinemia), adipose tissue glycerokinase activity was not elevated in comparison to lean control groups when expressed on a mg protein basis. It is concluded that the elevated glycerokinase activity is not due to the specific Db or Ob mutation, but is secondary to the obesity and hyperinsulinemia interacting with the similar genetic background in the C57BL/KsJ and the C57BL/6J mouse strains.
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PMID:Adipose tissue glycerokinase activity in genetic and acquired obesity in rats and mice. 16 46

The status of insulin-receptor interactions in a variety of insulin-resistant states is reviewed. Utilizing large adipocytes from adult rats and small fat cells from young rats, we have conducted a series of in vitro experiments in an attempt to determine the cellular alteration(s) responsible for the insulin resistance associated with obesity. Stimulation of glucose oxidation by insulin is reduced in large cells. Studies using a mimicker of insulin action, spermine, as well as measurements of 125I-insulin binding to large and small cells indicate that receptor number and affinity are not responsible for hormone resistance. Furthermore, when rapid and direct measurements of sugar uptake were made, insulin stimulation was virtually identical in both cell types. These findings indicate that large adipocytes have an efficient insulin-responsive D-glucose transport system and suggest that the apparent hormone resistance may be due to alterations in intracellular glucose metabolism. It has been proposed that altered insulin-receptor interaction underlies the insulin resistance of human obesity. We have investigated this particular aspect of insulin action by 125I-insulin binding studies. Similar numbers of insulin receptors per cell and affinity for insulin were observed in adipocytes obtained from normal weight subjects and morbidly obese patients. Thus, the initial step in insulin action is unaltered in human obesity.
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PMID:Relation of insulin receptors to insulin resistance. 16 83

A connecting link between carbohydrate and fat metabolism in adipose tissue is theconcentration of alpha-glycerophosphate derived predominantly from the glycolysis ofglucose entering the fat cell. However, several investigators have reported the presence of a glycerol specific kinase in the epidiymal fat-pad of the rat and obob mouse. This enzyme's presence in other mammalian adipose tissue could contribute to the alpha-glycerophosphate pool and thus affect both carbohydrate and fat metabolism within the fat cell. Glycerokinase was demonstrated in isolated fat cells obtained from the subcutaneous, perirenal, epididymal, and dorsal intrascapular brown fat depots of the adultmale rat. It was found to be particularly sensitive to in vivo lipogenic stimuli in both the subcutaneous and the brown adipose tissue and concluded that insulin is involved in adipose glycerokinase stimulation. Therefore, the main function of glycerokinase in normal adipose tissue may be to augment the anabolic action of insulin. It isfurther suggested that deviation from the normal control of this lipogenic enzyme couldlead to a gradual accumulation of fat and eventual obesity.
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PMID:Glycerokinase in mammalian adipose tissue: stimulation by lipogenic substances. 16 85

We have previously shown that in the insulin-resistant obese hyperglycemic mouse (ob/ob) there is a deficiency in the number of insulin receptor sites on hepatocytes, adipocytes, and thymic lymphocytes. We now find that concentration of insulin receptors on liver plasma membranes is decreased in the db/db mouse, another form of inherited obesity, and in normal mice that became obese after treatment with gold thioglucose, while thin mice, heterozygous for the ob mutation (ob/+), have normal insulin binding. With acute and chronic food restriction of the ob/ob and gold thioglucose obese mice, there is reduction in hyperinsulinemia and an associated increase in the insulin receptor concentration toward normal. In contrast, when fasting ob/ob mice were given exogenous insulin to maintain the hyperinsulinemia, insulin receptors failed to increase. Thus, in all cases, there was a consistent relationship between the degree of hyperinsulinemia and of insulin receptor loss. These findings suggest that decreased insulin binding is a characteristic feature of the insulin resistance of obesity, and that sustained hyperinsulinemia is a major factor in the control of the concentration of insulin receptors on target cells.
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PMID:Insulin receptor deficiency in genetic and acquired obesity. 16 96

The clinical and biochemical features of eleven patients with Type V hyperlipoproteinaemia have been reviewed. All patients were male, and there was a high incidence in the group of obesity, vascular disease, acute abdominal pain, gout, diabetes mellitus and alcoholism. Plasma cholesterol concentrations ranged from 212 to 1512 mg/100ml and triglycerides from 708 to 7670 mg/100 ml. Lipaemia was associated with significant hyponatraemia, and also interfered with the determination of plasma glucose and serum amylase. Chylomicronaemia and hyperprebetalipoproteinaemia were accompanied by reduction in the pools of beta and alpha lipoproteins. All lipoprotein classes were relatively depleted of cholesterol compared to triglyceride. There was a variable pattern of treatment response. In some patients alcohol withdrawal produced a rapid improvement in plasma lipids. In diabetes mellitus there were two types of response: a rapid one in chronic insulin deficiency, and secondly, a more gradual one in mild diabetes associated with hyperinsulinaemia. In other patients there was a rapid response to carbohydrate-calorie restriction but the respective contributions of each of the steps remained unclear.
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PMID:Type V hyperlipoproteinaemia re-visted: findings in a sydney population. 16 79

Insulin receptor concentrations in liver plasma membranes of New Zealand Obese (NZO) mice have been studied. When NZO mice were implanted with normal islets of Langerhans their blood glucose and plasma insulin declined. When the implanted islets were removed these changes were reversed and the mice reverted to their insulin resistant state. Changes were observed in the binding of 125I-insulin to liver plasma membranes of implanted NZO mice. Binding increased when the plasma insulin was decreased and conversely insulin binding decreased when the plasma insulin levels became elevated. The increased insulin binding was not accompanied by any changes in the affinity of NZO liver receptors for insulin.
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PMID:The control of insulin receptors in the New Zealand obese mouse. 17 9


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