In vivo hepatic and peripheral insulin resistance in genetically obese (fa/fa) rats.

@article{Terrettaz1983InVH,
  title={In vivo hepatic and peripheral insulin resistance in genetically obese (fa/fa) rats.},
  author={Jacques Terrettaz and Bernard Jeanrenaud},
  journal={Endocrinology},
  year={1983},
  volume={112 4},
  pages={
          1346-51
        },
  url={https://api.semanticscholar.org/CorpusID:24327050}
}
The aim of the study was to assess the in vivo relevance of previously described in vitro abnormalities of muscle and adipose tissues producing insulin resistance in genetically obese (fa/fa) rats and decide whether livers of obese rats were insulin resistant.
View on PubMed
doi.org
141 Citations
Highly Influential Citations
4
Background Citations
26
Methods Citations
14
Results Citations
1

141 Citations

Severe hepatic and peripheral insulin resistance as evidenced by euglycemic clamps in genetically obese fa/fa rats.

Studying in vivo the action of insulin on glucose metabolism and hepatic glucose production in lean and genetically obese rats suggests that basal plasma insulin levels appear to maximally stimulate peripheral glucose metabolism, and the presence of postreceptor defects prevents any further stimulatory effect of the hormone.

Insulin resistance in the Zucker diabetic fatty rat: a metabolic characterisation of obese and lean phenotypes

Obese animals showed significantly increased glucose incorporation into lipid in all of these tissues, indicating an increase in lipogenesis, and an integrated characterisation of in vivo insulin resistance in obese ZDF rats is presented.

Pathogenesis of hyperglycemia in genetically obese-hyperglycemic rats, Wistar fatty: presence of hepatic insulin resistance.

The present studies indicate that insulin resistance in the hepatic enzyme regulation may contribute to the development of hyperglycemia in Wistar fatty rats and changes in hepatic glycolytic intermediates supported this suggestion.

Insulin induces rapid changes of plasma leptin in lean but not in genetically obese (fa/fa) rats

The results suggest that insulin may be a regulator of in vivo leptin secretion by adipose tissue of lean rats whereas it is ineffective in increasing plasma leptin in obese Zucker rats.

Pancreatic hypersensitivity to glucose by young obese Zucker rats (fa/fa).

Decreased responsiveness of basal gluconeogenesis to insulin action in hepatocytes isolated from genetically obese (fa/fa) Zucker rats.

In hepatocytes isolated from obese (fa/fa) rats, neither basal gluconeogenesis nor any of the other metabolic parameters mentioned were significantly modified by insulin, even when assayed at high hormonal concentrations.

Abnormal oral glucose tolerance in genetically obese (fa/fa) rats.

Irrespective of age, the obese rats had a normal blood glucose tolerance when glucose or tolbutamide load was given intravenously, whereas the glucose ingestion [oral glucose tolerance test (OGTT) caused a marked glucose intolerance that became more pronounced with the duration of the syndrome.

Metabolic abnormalities of the hyperglycemic obese Zucker rat.

Mechanism of Abnormal Oral Glucose Tolerance of Genetically Obese fa/fa Rats

The aim of this study was to investigate the mechanism(s) underlying the abnormal oral glucose tolerance test of obese animals with the non-steady-state measurement of glucose turnover proposed by Steele et al. in 1968, and show that the total rate of glucose appearance is enhanced in obese compared with lean animals.

Central nervous system and peripheral abnormalities: clues to the understanding of obesity and NIDDM

The data suggest that the aetiology of obesity-insulin resistance of genetically obese rodents has to be searched within the brain, not peripherally.
...

12 References

Glucose metabolism and recycling of radioactively labelled glucose in the Zucker genetically obese rat (fa/fa).

There was no difference in the proportion of 14C (derived from metabolized labelled glucose) that recycled as [14C]-glucose after passing through the pyruvate pool in the two groups of rats if the rate of recycling of radioactivity was expressed as a percentage of R0.

The Zucker-fatty rat: a review.

A model is presented in which the features of the genetically obese (Zucker) fatty rat are compared with those of animals with hypothalamic obesity, which includes hyperinsulinemia, reduced levels of glucagon, hypothyroidis, and impaired reproductive function.

Mechanism of control of hepatic glycogenesis by insulin.

Glucose clamp technique: a method for quantifying insulin secretion and resistance.

Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique) are described.…

Influence of hyperinsulinemia, hyperglycemia, and the route of glucose administration on splanchnic glucose exchange.

It is suggested that orally consumed glucose causes the release of a gastrointestinal factor that enhances insulin-mediated glucose uptake by the liver and causes minimal net uptake of glucose by the splanchnic bed despite marked stimulation of total glucose turnover.

Dose-response characteristics for effects of insulin on production and utilization of glucose in man.

The above dose-response relationships indicate that in man glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; both hepatic and peripheral tissues may contain "spare" insulin receptors; and relatively minor changes in Plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism.

Determination of synthesis, recycling and body mass of glucose in rats and rabbits in vivo 3H-and 14C-labelled glucose.

The curve of total body glucose radioactivity was obtained from the (3)H(2)O yield, and total mass of glucose was calculated, which agrees with that obtained with the ( 3)H specific-radioactivity curve.

Glycogen synthesis by rat hepatocytes.

Glycogen synthesis increases with glucose concentrations attaining maximal values at 50--60mM, when it is similar to that obtained in the presence of 10mM glucose and lactate plus glutamine, and phosphorylase activities increased during glycogen syntheses, while in glycogen synthesis from glucose as sole substrate there was a decline in phosphate activities with increased glucose concentration and increased rates of glycogen deposition.

Glycogen synthesis in isolated parenchymal rat liver cells

Insulin regulation of glycogen synthase in the isolated rat hepatocyte.