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

The weighing of the human body under water is an application of Archimedes' law. Fat being lighter than water or than the structures of lean body mass, body fat can be measured by determining the specific gravity of the human body; that is, by underwater weighing. Body fat has been determined in an "ideal" sample of 14 men and 23 women, all aged 20 years. Testing against a reference measure of body fat makes it possible to test the validity of some anthropometric measurements and of some indices of obesity. These indices offer no advantages over anthropometric measurements.
Schweiz Med Wochenschr 1978 Dec 02
PMID:[Measurement of human body fat by means of gravimetry. Application of Archimedes' principle]. 71 34

Small doses of the opiate antagonist naloxone selectively abolished overeating in genetically obese mice (ob/ob) and rats (fa/fa). Elevated concentrations of the naturally occurring opiate beta-endorphin were found in the pituitaries of both obese species and in the blood plasma of the obese rats. Brain levels of beta-endorphin and Leu-enkephalin were unchanged. These data suggest that excess pituitary beta-endorphin may play a role in the development of the overeating and obesity syndrome.
Science 1978 Dec 01
PMID:beta-Endorphin is associated with overeating in genetically obese mice (ob/ob) and rats (fa/fa). 71 55

Displacement of the right kidney, simulating crossed renal ectopia, was associated with massive obesity and a ventral hernia.
J Can Assoc Radiol 1978 Dec
PMID:Renal displacement simulating crossed renal ectopia. 72 85

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.
Metabolism 1978 Dec
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.
Metabolism 1978 Dec
PMID:Hyperinsulinemia in obesity syndromes: its metabolic consequences and possible etiology. 72 39

Obese female Zucker rats show persistent increases in fat cell number compared to lean female Zucker rats from 5 to 52 wk of age. The hyperplastic obesity of the Zucker rat is also accompanied by fat cell hypertrophy and elevated plasma immunoreactive insulin (IRI). Average adipocyte size reaches a peak value at 14 wk of age in the subcutaneous, retroperitoneal and parametrial depots of the female obese rat. Plasma IRI also shows a peak at 14 wk of age. In addition, at this age thymidine kinase activity, a measure of proliferative capacity in tissue, is elevated in obese compared to lean rats, and at 15 1/2 wk of age a bimodal distribution of adipocytes is present in obese rat adipose tissue. The data suggest that attainment of a critical adipocyte size accompanied by maximum levels of plasma IRI may act in concert to potentiate fat cell hyperplasia in Zucker obese rats.
Metabolism 1978 Dec
PMID:Adipose tissue hyperplasia and hyperinsulinemia on Zucker obese female rats: a developmental study. 72 43

Lipoprotein lipase (LPL) enzyme activity in epididymal adipose tissue from obese and lean Zucker rats was measured. At 5, 10, 13, and 20 wk of age obese rats have heavier fat pads, larger fat cells, and more LPL per epididymal fat pad and per fat cell than do their lean littermate controls. Although LPL per fat cell increased as fat cell size increased in lean rats, the increased LPL activity in the obese could not be attributed solely to increased fat cell size. When obese and lean rats had similar cell sizes, LPL per fat cell was still significantly increased in the obese compared to lean. Furthermore LPL activity was increased in "preobese" (fa/fa) rats compared to either lean genotype (Fa/fa or Fa/Fa) during the second postnatal week. The data suggest that early increments in LPL activity in adipose tissue of the "pre-obese" rat may significantly contribute to the early fat cell hypertrophy seen during the development of this genetic obesity. Furthermore, early increased LPL activity may prove useful as a predictor of the onset of obesity.
Metabolism 1978 Dec
PMID:Increased adipose tissue lipoprotein lipase activity during the development of the genetically obese rat (fa/fa). 72 44

Isolated fat cells derived from 10-wk-old Zucker obese rats utilized substantially greater amounts of glucose per cell in the presence or absence of insulin than those from lean rats. Initial rates of deoxyglucose or 3-0-methylglucose uptake in fat cells from Zucker obese rats were also 5--10 times greater than those observed in cells from lean rats. However, while 240 microU/ml insulin elicited a maximal response in fat cells from lean rats, this dose of hormone was only about 50% as effective as 24 microU/ml insulin in stimulating glucose metabolism or hexose transport in obese rat cells. This apparent rightward shift in the dose response-relationship could not be adequately explained on the basis of decreased insulin receptors since (125I-) insulin binding per fat cell was increased 2.5--3-fold in obesity, while receptor density on the cell surface in obesity was decreased only slightly. Soleus muscles from obese Zucker rats exhibited decreased basal rates of D(5-3H)glucose conversion to glycogen and H2O compared to those of lean controls. While the percent increase in glucose metabolism due to a supermaximal dose of insulin was similar in soleus muscles of lean and obese Zucker rats, a blunted response to a submaximal insulin dose was observed in muscles from the latter animals. This rightward shift in the dose-response relationship was also observed when deoxyglucose uptake was monitored in soleus muscles from obese rats. Binding of (1251-) insulin to soleus muscles at a medium concentration of 57 microU/ml was significantly decreased in obese compared to lean rats. We conclude that (1) fat cells do not contribute to the insulin resistance of 10-wk obese Zucer rats since glucose utilization is higher in these cells at all concentrations of insulin tested, (2) obese Zucker rat soleus muscle metabolism is defective in two respects--imparied basal glucose utilization and a rightward shift in the insulin dose-response relationship with respect to hexose transport, and (3) this latter defect involving decreased sensitivity of muscle to insulin appears to result from a marked decrease in cell surface receptors for the hormone.
Metabolism 1978 Dec
PMID:Insulin response in skeletal muscle and fat cells of the genetically obese Zucker rat. 72 45

The isolated mouse soleus muscle is a suitable system to measure specific insulin binding and insulin effects. Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. These alterations are responsible for the marked resistance to maximally stimulating doses of insulin. The serum from a patient with the syndrome of insulin resistance and acanthosis nigricans contains antibodies that inhibit insulin binding and exert insulin-like effects in muscle; this serum is, however, less effective than insulin in maximally stimulating glycogen synthesis, which suggests some differences in their mechanisms of action.
Metabolism 1978 Dec
PMID:Studies of insulin insensitivity in soleus muscles of obese mice. 72 46

Effects of insulin (1 mU/ml) on diaphragms removed from older-obese (70--110 days, 350--520 g) male Sprague-Dawley rats were compared to responses on muscle removed from younger-lean (27--36 days, 80--150 g) animals. Insulin antagonism on glucose transport (2DG uptake), glucose uptake, glycogen synthesis, glycolysis (lactate production), and glucose oxidation was demonstrated in tissue from the older-obese rats. Extracellular water spaces (measured with inulin-H3) were significantly decreased in these tissue. To determine if insulin antagonism of glucose transport could be secondary to inhibition of a rate-limiting reaction in the Embden-Meyerhof pathway with a subsequent negative feedback on transport, both tissue levels of glycolytic intermediates and oxidation of intracellular lipids were measured. No free intracellular glucose was found in diaphragms from either group of rats. Levels of G-6-P, F-6-P, F-1, 6-diP, PEP, and pyruvate were all lower in muscle from the older-obese animals. Incorporation of C14-FFA into tissue TG was slightly, but significantly, lower in this same tissue. Oxidation of intracellular TG and PL was similar in the two groups. In conclusion, diaphragms from older-obese rats manifest insulin antagonism of glucose transport that is probably responsible for the diminished hormonal effect on glucose uptake and the intracellular pathways of glycogen synthesis, glycolysis, and glucose oxidation. This inhibition of insulin action cannot be accounted for by changes in glycolytic intermediates causing a negative feedback on transport or enhanced lipid oxidation and therefore should be considered primary. The relative effects of age and obesity will need to be evaluated in future studies.
Metabolism 1978 Dec
PMID:Primary insulin antagonism of glucose transport in muscle from the older-obese rat. 72 47


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