Journal ArticleDOI
Effects of Chronic Vanadate Administration in the STZ-Induced Diabetic Rat: The Antihyperglycemic Action of Vanadate Is Attributable Entirely to Its Suppression of Feeding
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The glucose-lowering effect of vanadate in STZ-induced diabetic rats can be explained by its inhibition of feeding, and its hypophagic action does not appear to involve inhibition of NPYergic pathways in the hypothalamus.Abstract:
Vanadate treatment can lower glycemia in diabetic rats. This action is generally attributed to vanadate's insulinomimetic properties, but vanadate also inhibits feeding, which could lower blood glucose. We therefore assessed the contribution of hypophagia to vanadate's antihyperglycemic action in a 3-week study of streptozocin-induced (STZ) diabetic rats. Untreated diabetic rats ( n = 8) ate 54% more food than nondiabetic control rats ( P 0.05 vs. vanadate-treated diabetic rats). Vanadate treatment did not affect plasma insulin concentrations in diabetic rats. In nondiabetic rats ( n = 8), vanadate treatment significantly reduced food intake ( P < 0.05) and also lowered plasma insulin concentrations ( P < 0.05) without significantly affecting glycemia. To investigate the mechanism of vanadate's hypophagic effect, we also measured regional hypothalamic levels of neuropeptide Y (NPY), a potent central appetite stimulant that is thought to drive hyperphagia in STZ-induced diabetes. Hypothalamic NPY concentrations rise markedly in diabetes and are normalized by insulin replacement. Unlike insulin, vanadate treatment did not normalize regional hypothalamic NPY concentrations in diabetic rats. Vanadate does not therefore appear to exert an insulin-like action at the hypothalamic level; its hypophagic action does not appear to involve inhibition of NPYergic pathways in the hypothalamus. We conclude that the glucose-lowering effect of vanadate in STZ-induced diabetic rats can be explained by its inhibition of feeding. Although vanadate has certain insulinomimetic effects in vitro and in vivo, the role of these effects in vanadate's antidiabetic actions must be critically reexamined.read more
Citations
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Journal ArticleDOI
Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin-dependent diabetes mellitus.
TL;DR: It is indicated that 3 wk of treatment with vanadyl sulfate improves hepatic and peripheral insulin sensitivity in insulin-resistant NIDDM humans.
Journal ArticleDOI
Metabolic effects of sodium metavanadate in humans with insulin-dependent and noninsulin-dependent diabetes mellitus in vivo and in vitro studies
TL;DR: The data suggest that vanadate or related agents may have a potential role as adjunctive therapy in patients with diabetes mellitus.
Journal ArticleDOI
Insulino-mimetic and anti-diabetic effects of vanadium compounds.
Ashok K. Srivastava,M. Z. Mehdi +1 more
TL;DR: Compounds of the trace element vanadium exert various insulin‐like effects in in vitro and in vivo systems and are suggested to enhance insulin signalling and action by virtue of its capacity to inhibit PTPase activity and increase tyrosine phosphorylation of substrate proteins.
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Oral vanadyl sulfate improves insulin sensitivity in NIDDM but not in obese nondiabetic subjects
TL;DR: Small oral doses of vanadyl sulfate do not alter insulin sensitivity in nondiabetic subjects, but it does improve both hepatic and skeletal muscle insulin sensitivity during three-hour euglycemic-hyperinsulinemic clamps in NIDDM subjects in part by enhancing insulin's inhibitory effect on lipolysis.
Journal ArticleDOI
The role of vanadium in the management of diabetes.
TL;DR: In vitro, vanadium salts mimic most effects of insulin on the main target tissues of the hormone, and in vivo they induce a sustained fall in blood glucose levels in insulin-deficient diabetic rats, and improve glucose homeostasis in obese, insulin-resistant diabetic rodents.
References
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Journal ArticleDOI
Neuropeptide Y chronically injected into the hypothalamus: a powerful neurochemical inducer of hyperphagia and obesity.
TL;DR: These findings, demonstrating that exogenous NPY is capable of overriding mechanisms of satiety and body weight control, suggest that disturbances in NPY function may play a role in some disorders of eating behavior and body Weight regulation.
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Insulin in the brain: a hormonal regulator of energy balance.
TL;DR: Recent investigations indicate that “brain insulin” is derived largely from the circulation, and a growing body of evidence suggests that its delivery into the neuropil may be facilitated by a specialized BBB barrier.
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Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats
TL;DR: Cardiac performance was depressed in the untreated diabetic animals, but the cardiac performance of the vanadate-treated diabetic animals was not significantly different from that of nondiabetic controls, so vanadates controlled the high blood glucose and prevented the decline in cardiac performance due to diabetes.
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Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food
TL;DR: Findings of intense and dynamic NPY neurosecretory activity within a discrete hypothalamic site in association with an increased drive for food consumption demonstrate that NPY release in the PVN is an important orexigenic signal for periodic eating behavior.
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Neuropeptide Regulation of Appetite and Weight
TL;DR: The role of peptides as modulators of feeding behavior and weight regulation is focused on and peptides synthesized and released in the central nervous system and act as neurotransmitters are studied.