Effects of the electric stress on insulin secretion and glucose metabolism in rats fed with a high fat diet.

Abstract

The synergetic effects of dietary obesity and stress induced by electrical shocks on insulin secretion from the perfused pancreas, the action of insulin on adipose tissues and glucose tolerance were studied in rats. The rat was fed either a control (C) (50% starch) or a high fat diet (F) (40% butter) for a period of 12 weeks. Half of the rats on each diet received electrical shocks, one hour per day for the last three weeks of the experiment (group C-S, F-S). The remaining rats were not given any stress sessions (group C-N, F-N). The rats on the high fat diet gained a significant amount of weight at the 8th week, and as determined by the adipocytes, were obese at the end of 12 weeks. However, the high fat diet itself did not have any effect on plasma glucose, plasma insulin and insulin release from the perfused pancreas in response to glucose. It caused glucose intolerance and the insensitivity to insulin of adipose tissue. The rats which received electrical shocks stopped gaining weight when the shock sessions began. Moreover, the size of the adipocytes in F-S group was significantly smaller than that in F-N group, but the insensitivity to insulin of adipose tissue remained. In F-S group, glucose-induced insulin release from the perfused pancreas was signiffcantly diminished in the initial phase of release, and glucose tolerance was much impaired by stress, while in C-S group insulin release increased in the late phase of release, and glucose tolerance was unaffected by stress. These findings indicate that the ability of glucose to stimulate insulin secretion is decreased by the synergetic effects of a high fat diet and stress induced by electric shock. Thus, it may be concluded that the mechanism which mediates the effects of glucose upon insulin secretion, especially in the initial response phase, is modified by such synergetic effects.

Opposite effects of short- and long-term fatty acid infusion on insulin secretion in healthy subjects

“…Numerous studies have shown that acute increases in plasma NEFA concentrations are associated with a stronger beta-cell response to glucose [1,2]. In contrast, only few and conflicting data have been reported regarding long-term exposure of beta cells to high plasma NEFA concentrations [16][17][18].…”

The Combination of a High-fat Diet and Chronic Stress Aggravates Insulin Resistance in Wistar Male Rats

“…The combination of chronic stress and a high-fat diet consistently produces adverse eff ects on behavioral and physiological responses. Studies on animals have shown that the combination of chronic stress and a high-fat diet produces synergistic eff ects on physiological measures, including increased stress-induced mortality and cardiovascular disorders [6,7] , inhibition of insulin secretion [8,9] , disruption of metabolic neuroendocrine balance [10] , retraction of hippocampal dendrites [11] and excessive activation of the hypothalamo-pituitary-adrenal (HPA) axis [12] . It is generally accepted that resistance to insulin mainly displays in target tissues, such as liver, adipose and skeletal muscle, especially in the liver [13] .…”

Stress- and age-related serum glucose changes in Spontaneously Hypertensive and Sprague-Dawley rats

“…In that regard, the present results agree with those of Ehrentheil et al (1967) and Wexler (198\). Presumably, exposure to the unpredictable, uncontrollable grid shocks results in sympathetic activation and release of catecholamines , glucocorticoids (Berger, Starzec, & Mason, 1981), inhibition of insulin release (Mason, 1968;Yamaguchi et al, 1978), and other changes which produce an elevation in serum glucose. These effects are exaggerated in the SHR .…”

“…The SHRs were maintained on a highlipid diet as part of our work on the effects of psychological stress on cholesterol metabolism. Therefore, relatively higher glucose levels were expected because of the synergistic action of the diet and stress (Yamaguchi, Takashima, Masuyama, & Matsuoka, 1978). It was expected that stress would result in elevated serum glucose, and that the old, stressed SHRs would have the highest levels.…”