Amelioration of insulin resistance in obese mice

Mahler, Richard J.; Szabó, Olga

doi:10.1152/ajplegacy.1971.221.4.980

Cited by 54 publications

(24 citation statements)

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“…Mahler and Szabo [9] have shown that it is possible to get reversion of ob/ob characteristics by controlled treatment of suggest that the change in peripheral receptors could occur as a result of hyperinsulinaemia, reinforcing the previous suggestion that hypersecretion of insulin may be a primary fault. It has been shown that there is a close relationship between the functioning of e-and fl-cells in the islets [12].…”

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confidence: 60%

Further studies on the amelioration of the characteristics of New Zealand Obese (NZO) mice following implantation of islets of Langerhans

1974

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Summary. New Zealand Obese (NZO) mice are eharaeterised by hyperglyeaemia, hyperinsulinaemia and obesity. The blood glucose and plasma insulin levels of these mice can be lowered to levels approaching those normally associated with non-obese mice, by the intraperitoneal implantation of pancreatic islets from albino mice which have had their fl-cells selectively destroyed by streptozotocin. Removal of these implanted islets causes the animals to revert to their original state. It would seem, therefore, that the genetic lesion responsible for the NZO state lies within the islets of Langerhans but not within the beta-cell. Its exact location is as yet unknown.

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confidence: 60%

Further studies on the amelioration of the characteristics of New Zealand Obese (NZO) mice following implantation of islets of Langerhans

1974

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“…In the homozygous ob/ob mouse, marked islet cell hypertrophy in association with extremely high plasma insulin levels is seen with increasing adiposity while the blood sugar is normal and peripheral tissue responsivity to insulin is preserved and may, in fact, be increased (32,33). Suppression of pancreatic islet hyperplasia with alloxan restores the in vivo insulin sensitivity in the obese mice (40). Similarly, hyperinsulinemia has been demonstrated in the obese Zucker rat prior to the onset of peripheral insulin resistance (41).…”

Section: Resultsmentioning

confidence: 98%

Splanchnic insulin metabolism in obesity. Influence of body fat distribution.

Peiris¹,

Mueller²,

Smith³

et al. 1986

J. Clin. Invest.

323

143

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The effects of obesity and body fat distribution on splanchnic insulin metabolism and the relationship to peripheral insulin sensitivity were assessed in 6 nonobese and 16 obese premenopausal women.When compared with the nonobese women, obese women had significantly greater prehepatic production and portal vein levels of insulin both basally and following glucose stimulation. This increase correlated with the degree of adiposity but not with waist-to-hip girth ratio (WHR). WHR, however, correlated inversely with the hepatic extraction fraction and directly with the posthepatic delivery of insulin. The latter correlated with the degree of peripheral insulinemia. The decline in hepatic insulin extraction with increasing WHR also correlated with the accompanying diminution in peripheral insulin sensitivity.Increasing adiposity is thus associated with insulin hypersecretion. The pronounced hyperinsulinemia of upper body fat localization, however, is due to an additional defect in hepatic insulin extraction. This defect is closely allied with the decline in peripheral insulin sensitivity.

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“…Whereas many prior studies have established that insulin-stimulated glucose uptake or metabolism of muscle from the oblob mutation is decreased in vitro (31)(32)(33)(34)(35) Conditions were as described in Tables II, IV, and VI, except that 4% bovine albumin was used. [5-3H]glucose (sum of both glycogen synthesis and glycolysis), and decreased 2-deoxyglucose accumulation, all in the absence of insulin, and after two preincubations to remove whatever insulin might have been present in the tissue at death.…”

Section: Discussionmentioning

confidence: 99%