Insulin Sensitivity in Rats with Ventromedial Hypothalamic Lesions

Hongslo, Cecilie F.; Hustvedt, Bo-Egil; Lövö, Arne

doi:10.1111/j.1748-1716.1974.tb05644.x

Cited by 7 publications

(7 citation statements)

References 19 publications

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“…Similarly, the same or similar central areas can exert control over the internal metabolic milieu (16)(17)(18)(19)(20)(21)(22). Pathways through which these latter effects could be mediated include direct autonomic nervous system control over tissue metabolism (23)(24)(25)(26) and direct control mediated through autonomic nervous system modification of hormonal release (18-21, 23, 26-31).…”

Section: Introductionmentioning

confidence: 99%

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Burr¹,

Slonim²,

Sharp³

1976

J. Clin. Invest.

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A B S T R A C T An in vitro system for perifusion of rat pancreatic islets has been utilized to define the effects of epinephrine on acetylcholine-induced insulin release over varying concentrations of the two agents. Perifusion of islets with epinephrine before challenge with acetylcholine produced marked enhancement of both phases of cholinergically induced insulin release; enhancement of the first phase being more marked with increase in acetylcholine concentration and the converse being observed with the second phase. Perifusion of islets with epinephrine during stimulation with acetylcholine produced inhibition of insulin release, an effect dependent upon the concentration of epinephrine and of acetylcholine. There was an order of difference in the acetylcholine concentration needed to overcome significant epinephrine-mediated inhibition of the first phase of insulin release (5 X 10' Ag/ml) and that needed to overcome inhibition of the second phase (5 X 10-' g/ ml). Comparison of the effects of various concentrations of epinephrine on glucose-and acetyl-choline-induced insulin release revealed that epinephrine was a less potent inhibitor of the first phase of acetylcholine-induced insulin release than of the first phase of glucose-induced insulin release. These data provide some insight into the potential interactions between cholinergic and adrenergic autonomic systems in modifying insulin release.

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Section: Introductionmentioning

confidence: 99%

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Burr¹,

Slonim²,

Sharp³

1976

J. Clin. Invest.

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“…In addition to the changes in glucose and lipid metabolism discussed above, VMH destruction also affects protein metabolism, as shown by the increased plasma urea of the lesioned animals in this and other studies (7,12). This catabolic effect has been clearly demonstrated in nitrogen balance experiments (11).…”

Section: Discussionmentioning

confidence: 55%

“…Possibly, such a disturbance could also be responsible for the observed alterations in the pancreatic endocrine function, as discussed in a previous report (12). VMH-lesioned animals are reported to have normal insulin sensitivity (3,12). The marked hypoglycemia during the feeding period, relative to the control groups, is therefore probably due to an increased rate of glucose uptake from the plasma, caused by the hyperinsulinemia.…”

Section: Discussionmentioning

confidence: 80%

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The Effect of Ventromedial Hypothalamic Lesions on Metabolism and Insulin Secretion in Rats on a Controlled Feeding Regimen

Hustvedt

Lövö

Reichl³

1976

Ann Nutr Metab

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The metabolic effect of ventromedial hypothalamic (VMH) lesions, which are known to cause hyperphagia and obesity, has been studied in rats kept on a controlled light and food regimen. The animals were sacrificed at 4 different times during the second postoperative day. A feeding-induced hypersecretion of insulin was found in the VMH-lesioned animals. It was accompanied by a marked hypoglycemia as compared to the control groups during the feeding period. The glycogen content of liver and diaphragm in the lesioned groups is increased as compared to the controls during the same period. The VMH-lesioned animals showed hypertriglyceridemia both in the fed and fasted state, whereas the postabsorptive plasma levels of free fatty acids and glycerol were decreased. An increased level of urea was observed in all lesioned groups. This is in accordance with the demonstrated protein catabolism which follows VMH lesions.

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“…Fat cells from obese rats have a decreased capacity to incorporate glucose into fatty acids [11][12][13][14], suggesting that the low insulin responsiveness might be caused by a post-receptor defect due to changes in certain metabolic pathways. Low responsiveness to insulin without hyperinsulinaemia is found in experimental diabetes [15][16][17] and a normal response to insulin in association with hyperinsulinaemia is described in ventromedial hypothalamic (VMH) lesioned rats [18,19].…”

mentioning

confidence: 99%

Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding

Hansen¹,

Nilsson²,

Sonne

et al. 1983

Diabetologia

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Insulin resistance was studied by comparing insulin response and insulin binding in four groups of rats. Glucose metabolism in isolated fat cells from male Wistar rats weighing 340 g was less responsive to a supramaximal dose of insulin than glucose metabolism in fat cells from rats weighing 200 g. Induction of streptozotocin-diabetes in rats weighing 200 g resulted in a marked decrease in the insulin responsiveness of fat cells. Ventromedial hypothalamic lesions of 340 g rats had the opposite effect and restored the insulin responsiveness of fat cells. The responsiveness in the four groups was correlated to the rate of glucose conversion to fatty acids in fat cells. The binding of 125I-insulin was the same in both 340 and 200 g rats. The ventromedial hypothalamic lesioned rats and the diabetic rats showed, in spite of their great difference in insulin responsiveness, the highest binding of 125I-insulin to fat cells. Insulin binding was not correlated to the plasma insulin level which however was reflected in the lipoprotein lipase activity in the adipose tissue. In conclusion, these results indicate that variations in insulin responsiveness in fat cells are due to alterations in cellular metabolism rather than in insulin binding.

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Insulin Sensitivity in Rats with Ventromedial Hypothalamic Lesions

Cited by 7 publications

References 19 publications

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

The Effect of Ventromedial Hypothalamic Lesions on Metabolism and Insulin Secretion in Rats on a Controlled Feeding Regimen

Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding

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