Showing papers on "Insulin resistance published in 1972"
TL;DR: The presence of cirrhosis, a family history of diabetes and direct damage to the pancreas by iron deposition may all be involved in the development of diabetes in haemochromatosis, which might explain why only some of the patients with diabetes showed improvement in carbohydrate tolerance following venesection therapy.
145 citations
TL;DR: Under identical conditions of purification and incubation, plasma membranes of the obese mouse bind only 16–35% as much 125I-insulin as membranes ofThe thin mouse, in contrast to other characteristics of the membrane which are similar to these two animals.
104 citations
TL;DR: The results indicate that the defect responsible for this insulin-resistant state exists in a step subsequent to insulin binding, possibly in transmission of the insulin-receptor "signal" since insensitivity occurs under conditions where glucose transport and oxidative processes are not apparently impaired.
Abstract: Large insulin-insensitive adipocytes from adult rats have normal binding capacities and affinities for insulin. Diminished insulin-like responses to spermine and reduced rates of glucose oxidation are also evident in these cells. The results indicate that the defect responsible for this insulin-resistant state exists in a step subsequent to insulin binding, possibly in transmission of the insulin-receptor "signal" since insensitivity occurs under conditions where glucose transport and oxidative processes are not apparently impaired.
96 citations
TL;DR: Serum immunoreactive insulin levels (IRI) and insulin sensitivity were studied in lean, genetically obese “fatty” rats, and rats that became obese following hypothalamic lesions and Histologic changes in the appearance of islet tissue were described.
Abstract: Serum immunoreactive insulin levels (IRI) and insulin sensitivity were studied in lean, genetically obese “fatty” rats, and rats that became obese following hypothalamic lesions. Serum IRI was increased in obese “fatty” rats at 6 wk, 4 mo, and 11 mo of age. Similar increases were observed in hypothalamic lesioned (HTL) obese rats. Histologic changes in the appearance of islet tissue were described. Insulin sensitivity was studied in both “fatty” and HTL rats after a 19-hr fast. Genetic, but not regulatory, obesity was accompanied by insulin resistance. Possible reasons for this difference are discussed.
90 citations
TL;DR: Zucker obese rats are normoglycemic, hyperinsulinemic, and release more insulin from isolated pancreatic islets than do their nonobese controls, and a role for adipocytes in determining pancreatic function is suggested.
Abstract: SummaryZucker obese rats are normoglycemic, hyperinsulinemic, and release more insulin from isolated pancreatic islets than do their nonobese controls. Basal glucose conversion to glycogen by muscle and to CO2 by isolated adipocytes is similar in Zucker obese and nonobese; insulin resistance is present in both tissues in the obese. There is a significant correlation between adipocyte response to insulin and pancreatic insulin release in obese and nonobese rats. The authors suggest a role for adipocytes in determining pancreatic function.
83 citations
TL;DR: Limiting the caloric intake of the obob and lean mice for 5 days brought about changes similar to those caused by parabiosis, attributed to the decrease in body weight of the obese parabiotic mice, probably as a result of a reduced caloric intake.
Abstract: Obese-hyperglycemic mice (obob) were parabiosed with lean littermates and body weight, blood glucose, serum insulin and triglycerides as well as insulin-sensitivity of diaphragm muscle and epididymal fat were determined on the 50th postoperative day. Single (non-parabiosed) mice and lean/lean, obob/obob parabiosed pairs served as controls. The mortality rate was highest among lean/obob and lowest among lean/lean pairs. The gain in body weight was also least among both partners of lean/obob pairs. Parabiosis had a small (lowering) effect on the blood glucose and serum insulin level of lean mice but it improved markedly the hyperglycemia of parabiotic obob in both obob/obob and obob/lean pairs; in the latter the serum insulin was also significantly decreased suggesting an improvement of the animal's sensitivity to insulin. In vitro studies involving incubation of diaphragm muscle and epididymal fat tissue in the absence and presence of insulin (1 mU/ml) revealed that while parabiosis had no effect on the tissue-sensitivity to insulin in lean mice, it increased that of obob joined with either obese or lean mice. These changes are attributed to the decrease in body weight of the obese parabiotic mice, probably as a result of a reduced caloric intake. Thus, limiting the caloric intake of the obob and lean mice for 5 days brought about changes similar to those caused by parabiosis.
20 citations
TL;DR: In the experiments reported here, a marked functional abnormality of the islets of Langerhans in vivo was observed, with no response of plasma insulin to glucose, glucagon and tolbutamide but a greatly exaggerated response to arginine.
Abstract: THE New Zealand obese (NZO) mouse is characterized by genetically determined obesity, accompanied by insulin resistance, glucose intolerance and hyperinsulinaemia1–4. The pattern of insulin release in response to stimuli has not been described. In the experiments reported here, a marked functional abnormality of the islets of Langerhans in vivo was observed, with no response of plasma insulin to glucose, glucagon and tolbutamide but a greatly exaggerated response to arginine. This observation of a selective defect of islet function not only has important implications concerning the normal physiology of insulin release but may also aid in understanding the evolution of the abnormalities of islet cell function in human diabetes5.
18 citations
TL;DR: Evidence for the presence of uric acid abnormalities in acromegaly is equivocal, and the hyperuricemia seen post-adrenalectomy is related to the primary hypertensive state rather than to adrenal dysfunction.
14 citations
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12 citations
TL;DR: In this article, the influence of 2 weeks' treatment of 15 non-diabetic, obese subjects with 2 g of Metformin daily, on intravenous glucose tolerance and plasma insulin levels was studied.
Abstract: The authors have studied the influence of 2 weeks' treatment of 15 non-diabetic, obese subjects with 2 g of Metformin daily, on intravenous glucose tolerance and plasma insulin levels. Blood glucose fasting and during the IVGTT were not influenced by treatment, but the insulin levels and the insulin/glucose ratios were significantly decreased. This points to a decreased insulin resistance.
9 citations
TL;DR: Since BDF is similar to the diabetogenic protein isolated from the urine of patients withlipoatrophic diabetes, its lipid-mobilizing action might help to explain the lipoatrophy, hyperlipaemia, diabetes mellitus, and insulin resistance seen in lipoatrophic diabetic patients.
TL;DR: Investigations attempting to explain the pathogenesis of coexisting lipoatrophy, hyper-lipemia, insulin-resistant diabetes mellitus and hepato-splenomegaly and the pathogenetic hypothesis that humoral factors cause a constant increase in lipolysis and therefore prevent triglyceride storage in the adipocytes is discussed.
Abstract: A case of coexisting lipoatrophy, hyper-lipemia, insulin-resistant diabetes mellitus and hepato-splenomegaly (fatty liver and early cirrhosis, as shown by biopsy) is described. Investigations attempting to explain the pathogenesis of these disturbances are presented. From the urine of the patient both the insulin antagonizing (Louis' factor) and lipid mobilizing substance (Chalmers' factor) were extracted. Injection of these extracts obtained from the patient's urine induced 1) insulin resistance, 2) hyperlipemia and 3) fatty infiltration of the liver in mice. The pathogenetic hypothesis that humoral factors cause a constant increase in lipolysis and therefore prevent triglyceride storage in the adipocytes is discussed.
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TL;DR: In this paper, the hypothesis of local (tissue) factors being responsible for muscle tissue resistance to insulin in obese hyperglycemic mice (obobob) was investigated and neither the amount of fat nor the rate of insulin was found to be correlated with muscle resistance.
Abstract: The hypothesis of local (tissue) factors being responsible for muscle tissue resistance to insulin in obesehyperglycemic mice (obob) was investigated. Neither the amount of fat nor the rate of insulin
01 Jan 1972
TL;DR: The hypothesis of local (tissue) factors being responsible for muscle tissue resistance to insulin in obesehyperglycemic mice (obob) was investigated but neither the amount of fat nor the rate of insulin was investigated.
Abstract: The hypothesis of local (tissue) factors being responsible for muscle tissue resistance to insulin in obesehyperglycemic mice (obob) was investigated. Neither the amount of fat nor the rate of insulin
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TL;DR: Hiperglicemia, aumento of the tolerancia a la insulina y conspícuas modificaciones a cargo de las células A y B de las islas de Langerhans, anders que la glycémie et the tolérance à l'insuline restaient aux mêmes niveaux qu'on pouvait vérifier chez les animaux de contrôle non immun
Abstract: Hyperglycemia, increase of insulin tolerance and striking changes in B- and A-cells of the islets of Langerhans occurred in guinea pigs producing precipitating insulin antibodies after immunization with insulin in adjuvant. Treatment with cyclophosphamide inhibited the production of insulin antibodies while the blood sugar and insulin tolerance remained on the level of nonimmunized control animals. Also the islets of Langerhans were less severely injured than those of animals not treated with cyclophosphamide.
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TL;DR: Results indicate that one of the ways oestrogen may produce its action is by impairing a release of insulin from beta cells of the pancreas and that this in turn may set off a chain of biochemical reactions such as decreased glucose tolerance and increased lipolysis all of which may lead to the diabetic state.
Abstract: In order to investigate the exact mode of action of oral contraceptives on carbohydrate metabolism results of 6 months of oral administration of 1 mu-g/kg ethnyl oestradiol and 80 mu-g/kg megesterol acetate and of 1 mu-g/kg ethnyl oestradiol alone in female rabbits were studied. Glucose tolerance was impaired (high blood sugar concentration) by both the combined preparation and by the ethnyl oestradiol alone. Rats receiving the estrogen alone had impaired intravenous glucose tolerance and an increased level of circulating free fatty acids; hypoglycaemic response to tolbutamide was impaired both in severity and duration. The estrogenic component of oral contraceptives is suspected of playing the major role in causing alterations in carbohydrate metabolism. Results indicate that one of the ways oestrogen may produce its action is by impairing a release of insulin from beta cells of the pancreas and that this in turn may set off a chain of biochemical reactions such as decreased glucose tolerance and increased lipolysis all of which may lead to the diabetic state. A review of the literature on alterations in carbohydrate metabolism includes effects or oral contraceptives pregnancy and glucocorticoids on glucose tolerance and insulin response insulin resistance and pregnancy and the differential actions of pill components.