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At least 19 recordsLinked to original sources
PubMed1978

Longitudinal study on the establishment of insulin resistance in hypothalamic obese mice.

A longitudinal in vivo and in vitro analysis of the genesis of insulin resistance has been carried out in mice made obese by chemical made obese by chemical lesion (goldthioglucose, GTG) of the hypothalamus. Six weeks after GTG administration, glycemia and glucose disposal were normal but associated with increased insulin concentration, suggesting incipient insulin resistance. The in vitro counterpart of the latter in obese mice was observed in soleus muscle that was somewhat less responsive to insulin than controls, in liver that had increased basal lipogenesis but was uninfluenced by insulin, and in hepatic plasma membranes in which a slight decrease of insulin binding was measured. At this stage of obesity, basal adipose tissue lipogenesis was increased but the tissue responded in a normal fashion to insulin. These relatively discrete early metabolic changes were corroborated in vivo by a normal hypoglycemic effect of exogenous insulin. Sixteen weeks after GTG administration, hyperglycemia and gross hyperinsulinemia were recorded. This insulin resistance was evidenced in vivo by the lack of hypoglycemic effect of exogenous insulin unless considerable amounts of the hormone were administered. It coincided in vitro with a poor response of soleus muscle to insulin, an absence of a stimulatory effect of the hormone upon both adipose tissue and liver tissue, and a marked decrease in insulin binding to liver plasma membranes. It appears that insulin resistance is a multifactorial and progressive abnormality that might involve both insulin receptor and intracellular metabolic alterations.

Adipose Tissue↗
PubMed1979

Energy balances in obese mice.

According to most existing theories, the regulation of energy balance is achieved by control of energy intake. This study was undertaken to find out whether there was control of energy output as well. Food intake, energy balance and the feed efficiency of weanling female mice made obese with injections of gold-thioglucose and monosodium glutamate indicate that the obesity is primarly due to an increased energetic efficiency, and suggest that the hypothalamus plays a role in controlling energy output. In the case of treatment with MSG, a relative obesity was observed, i.e. an increase in body fat without any change in body weight. This indicates that the CNS centres for the regulation of body weight and body fat are probably not the same. It is suggested that MSG obesity will be a suitable model for comparative studies of body weight and the regulation of fat content. It is concluded that chemically induced obesity is due more to a lower metabolic rate than to an elevated food intake.

Animals↗
PubMed1977

Factors influencing insulin and glucagon secretion in lean and genetically obese mice.

The control of insulin and glucagon secretion from isolated pancreatic islets of lean and genetically obese mice has been compared. The enlarged islets of obese mouse pancreas and islets of obese mouse pancreas and islets of obese mice maintained on a restricted diet manifested a greater response to glucose stimulation of insulin secretion than the lean mice islets. The glucagon content of the islets, the secretion of glucagon in a medium containing 150 mg% glucose and the stimulation of glucagon secretion by arginine did not differ significantly in the two groups. Adrenaline stimulated glucagon secretion in vitro from obese mice but not from lean mice. Antinsulin serum injections into obese mice increased the plasma glucagon levels about twofold and had no effect on glucagon levels in lean mice, although the level of hyperglycaemia was the same in both groups. It is suggested that the suppression of glucagon release by glucose requires a higher concentration of insulin in the obese mouse pancreas than in lean mice.

Animals↗
PubMed1979

Somatostatin in the pancreas and hypothalamus of obese mice.

The pancreatic content of somatostatin, insulin, and glucagon and the hypothalamic content of somatostatin were examined in ob/ob mice at various ages and in goldthioglucose-obese mice. The total pancreatic content of somatostatin was increased in ob/ob mice compared to controls: 92 ng vs 75 ng (a 22% increase) at 2 months of age; 208 ng vs 131 ng (a 60% increase) at 6 months of age; and 184 ng vs 118 ng (a 60% increase) at 8 months of age. The total pancreatic content of glucagon in ob/ob mice was already enhanced by 70% over controls at 2 months of age (301 ng vs 173 ng) and did not increase further at later stages, whereas that of insulin progressively rose with age. In goldthioglucose-obese mice the pancreatic content of insulin was also increased but to a lesser extent than in ob/ob mice; the pancreatic levels of somatostatin and glucagon were unaltered. In both ob/ob mice (regardless of age) and goldthioglucose-obese mice, there was no significant change in the hypothalamic content of somatostatin compared with that of lean controls.

Aging↗
PubMed1979

Influence of norepinephrine and fasting on the oxygen consumption of genetically-obese mice.

Oxygen consumption was monitored in fed and fasted, lean and obese mice of the ob/ob strain before and after subcutaneous injections of norepinephrine (NE). The increase in oxygen consumption after NE was of a similar magnitude in both lean and obese fed mice, but of a longer duration in the obese. Prior fasting caused a diminution of the response in the lean but was associated with an enhanced response in the obese mice. Fasting also resulted in a significant depression of the resting oxygen consumption of the obese mice but not of the lean. The relevance of these findings to the inability of the obese mouse to withstand cold exposure and to the maintenance of the obese state is discussed.

Animals↗
PubMed1979

On the characteristics of mitochondrial monoamine oxidase in pancreas and adipose tissues from genetically obese mice.

The substrate specificity of mitochondrial monoamine oxidase (MAO) in pancreatic and adipose tissues of obese mice and their lean counterparts was determined. The pancreatic MAO of obese mice had a greater specific activity than that of the lean mice. The white adipose tissue MAO was found to be more active than the brown adipose MAO in both groups of mice. While there was no appreciable difference in the MAO activities of brown adipose tissues between obese and lean mice, the enzyme from the white adipose tissue of obese mice had a higher specific activity than that of the lean mice. The higher MAO activity in white adipose tissue was observed when tyramine or serotonin was employed as substrate but not with benzylamine. Examination of mitochondrial MAO from epididymal adipocytes revealed marked differences in the properties of the enzyme between whole adipose tissue and isolated adipocytes. The inhibition characteristics of MAO from these tissues were studied with the specific inhibitors clorgyline and deprenyl.

Adipose Tissue↗
PubMed1977

Glycogen metabolism and cyclic AMP levels in isolated islets of lean and genetically obese mice.

The levels of glycogen and cyclic AMP, incorporation of glucose into glycogen and activities of glycogen synthetase and phosphorylase were determined in pancreatic islets isolated from genetically obese mice and their lean litter-mates. Islets from obese mice had elevated glycogen levels, increased phosphorylase activity and an increased amount of glycogen synthetase in the physiologically more effective I-form, indicating an increased turnover of glycogen. There was no significant difference in cyclic AMP levels between islets of lean and obese mice, but inhibition of phosphodiesterase or stimulation of adenyl cyclase increased cyclic AMP levels more in obese than in lean mouse islets, indicating a more rapid turnover of cyclic AMP in the former. It is suggested that cyclic AMP stimulated phosphorolytic breakdown of glycogen may be one of the mechanisms responsible for the increased insulin secretory response to glucose observed in islets from genetically obese mice.

Animals↗
PubMed1977

The ability of pancreatic polypeptides (APP and BPP) to return to normal the hyperglycaemia, hyperinsulinaemia and weight gain of New Zealand obese mice.

Intraperitoneal injections of avian pancreatic polypeptide (APP) and bovine pancreatic polypeptide (BPP) are capable of returning to normal the hyperinsulinaemia, hyperglycaemia and weight gain of New Zealand obese mice. The lag glucose tolerance also becomes indistinguishable from normal. The mechanism whereby these polypeptides cause reversion is not known. Reversion can also be brought about by the intraperitoneal implantation of islets from white mice into New Zealand obese animals. The implanted islets secrete mouse pancreatic polypeptide. We conclude that the New Zealand obese syndrome arises from a genetic lack of mouse pancreatic polypeptide. We suggest that in humans a lack of pancreatic polypeptide might manifest as a syndrome analogous to that found in New Zealand obese mice.

Animals↗
PubMed1978

Insulin binding and effects in isolated soleus muscle of lean and obese mice.

To get some insight into the mechanisms of insulin resistance in obesity, insulin binding and biological effects were investigated in soleus muscles isolated from normal and obese mice. Basal and insulin-stimulated 2-deoxyglucose uptake were measured at the steady state of insulin binding. The results were consistent with the concept of spare receptors, i.e., maximal insulin effect was achieved when only about 20% of total receptors was occupied. When similar studies were applied to muscles of gold thioglucose obese or genetically obese (ob/ob) mice, and compared to lean controls: a) insulin binding was decreased; b) the insulin dose-response curve of 2-deoxyglucose uptake was shifted to the right; c) maximally insulin-stimulated 2-deoxyglucose uptake, glycolysis, and glycogen synthesis were markedly decreased. Insulin binding and effects returned toward normal after a 40-h fast in obese mice. These results point to two loci for the insulin resistance of skeletal muscle in obesity: 1) a decrease in the number of insulin receptors, which results in a diminished insulin sensitivity; and 2) one or more alterations beyond receptor that are responsible for the decreased responsiveness of the tissue to insulin and appear to play a major role in the insulin resistance of muscle in obesity.

Animals↗
PubMed1978

Studies on some thermogenetic enzymes in brown adipose tissue of genetically obese mice.

The effects of cold exposure on several enzymes in brown adipose tissue (BAT) were examined in two types of genetically obese mice (C57BL/6J-ob and C57BL/6J-Ay) and their thin litter mates. In the thin C57BL/6J mice, the activities of two alpha-glycerophosphate-generating enzymes i.e., glycerokinase (GK) and alpha-glycerophosphate dehydrogenase (GDH), increased in BAT at cold exposure. Resemble results were observed in the yellow obese mice (A(y) mice). Nevertheless, in the obese-hyperglycemic mice (ob mice) showing a poor resistancy to cold, the increases of these enzymes were not observed. In addition, the increase of lipase activity, observed in BAT of the thin litter mates, was also not observed in BAT of ob mice. The decrease of NEFA release from BAT at cold exposure and the prominentry high inhibition rate of lipase by M NaCl were observed also in ob mice. Then the qualitive change of BAT lipase may exist in ob mice.

Adipose Tissue, Brown↗
PubMed1979

Deficient collagen formation by obese mice in a standard wound model.

Poor healing was demonstrated in two different experimental models of diabetes mellitus. In one model, there was an absolute lack of insulin and in the other, a resistance to insulin. A review of the history of the results of surgery in diabetic patients shows that in the clinical situation, wound failure is associated with both a lack of insulin and a resistance to insulin. Thus, the causes of wound failure in diabetic patients include a failure of insulin to perform its normal role in healing. This does not exclude other causes such as "small vessel disease" as etiologic factors, but it does suggest that control of metabolic derangements is beneficial to healing in diabetic patients who undergo operation.

Animals↗