Reciprocal Influences of the Ventromedial and Lateral Hypothalamic Nuclei on Blood Glucose Level and Liver Glycogen Content

Shimazu, Takashi; Fukuda, Aoi; Ban, Tadanobu

doi:10.1038/2101178a0

Cited by 232 publications

(83 citation statements)

References 3 publications

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“…However, the influence of these liypothalamic centres on the absorption and utilization of nutrients has not been fully investigated, although tliere have been a number of reports in the literature which suggest that these centres perform a metabolic function over and above the mere control of the quantity of food and water consumed. Shimazu, Fukuda and Ban (1966) have reported that electrical stimulation of the ventromedial nucleus in the rat causes a breakdown in liver glycogen and a rise in blood sugar levels, which they suggest is due to a sympathetic eflcct as similar results were obtained by splanchnic nerve stimulation. This is supported by the findings of Ban (1967) and Reinert (1964) who attril)uted urethane induced hyperglycaemia to the activation of the hypothalamic sympathetic mechanism.…”

supporting

confidence: 66%

The Effects of Bilateral Destruction of the Hypothalanhc Feeding Centre on Fastinc Blood Sugar, Glucose Absorption and Glucose Tolerance in the Rat

1971

Aust J Exp Biol Med

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Summary. The effects of bilateral destruction of the bypotlialamic "feeding" centre on tbe fasting blood sugar level, glucose alworption and gluco.se tolerance in the rat were investigated. It wa.s found tbat lesions in this area do not directly influence the.se aspects of glucose metabolism.Bilateral lesions in the ' ft-edinji" centre produced a market! and protracted elevation of the glucose tolerance curve after iichuinistration of a shicose load. However, this eftect was evidently due to dehydration resulting from adipsiii. Dehydration produces the same type of glucose tolerance curve in control animals without hypothalamic lesion.s.INTRODUCTION. It ha.s lieen firmly established that the hypothalamus controls nutrient intake by a dual mechanism consisting of a "satiety" centre inhibiting food and water intake, situated in the ventromedial nucleus, and a 'feeding" centre stimulating food and water consumption, situated in the lateral h>'pothalamus (Aiiaiid. 1961). However, the influence of these liypothalamic centres on the absorption and utilization of nutrients has not been fully investigated, although tliere have been a number of reports in the literature which suggest that these centres perform a metabolic function over and above the mere control of the quantity of food and water consumed.

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supporting

confidence: 66%

The Effects of Bilateral Destruction of the Hypothalanhc Feeding Centre on Fastinc Blood Sugar, Glucose Absorption and Glucose Tolerance in the Rat

1971

Aust J Exp Biol Med

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“…It has been shown that hyperglycemia can be induced through electrical stimulation of splanchnic or hepatic nerves in animals that have undergone adrenalectomy and/or pancreatectomy (34,35). In addition, Shimazu, Fukuda, and Ban (36) have shown that stimulation of the VMH specifically results in increased hepatic glycogenolysis and gluconeogenesis. Combined with the current study, these data suggest the possibility of a direct neural link from the hypothalamus to the liver (and less likely the kidney) that is capable of significantly reversing the suppressive effect of hyperinsulinemia on endogenous glucose production.…”

Section: Discussionmentioning

confidence: 99%

Potential Role for AMP-Activated Protein Kinase in Hypoglycemia Sensing in the Ventromedial Hypothalamus

et al. 2004

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The mechanisms by which specialized glucose-sensing neurons within the hypothalamus are able to detect a falling blood glucose remain largely unknown but may be linked to some gauge of neuronal energy status. We sought to test the hypothesis that AMP-activated protein kinase (AMPK), an intracellular kinase purported to act as a fuel sensor, plays a role in hypoglycemia sensing in the ventromedial hypothalamus (VMH) of the Sprague-Dawley rat by chemically activating AMPK in vivo through bilateral microinjection, before performing hyperinsulinemic-hypoglycemic or hyperinsulinemic-euglycemic clamp studies. In a subgroup of rats, H3-glucose was infused to determine glucose kinetics. The additional chemical activation by AICAR of AMPK in the VMH during hypoglycemia markedly reduced the amount of exogenous glucose required to maintain plasma glucose during hypoglycemia, an effect that was almost completely accounted for by a three-to fourfold increase in hepatic glucose production in comparison to controls. In contrast, no differences were seen between groups in hypoglycemia-induced rises in the principal counterregulatory hormones. In conclusion, activation of AMPK within the VMH may play an important role in hypoglycemia sensing. The combination of hypoglycemiaand AICAR-induced AMPK activity appears to result in a marked stimulus to hepatic glucose counterregulation.

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“…It has been demonstrated in several species that electrical stimulation of the splanchnic or hepatic nerves results in hyperglycemia, in spite of adrenalectomy and pancreatectomy (41,42). Stimulation of the ventromedial hypothalamus results in enhancement of hepatic glycogenolysis and gluconeogenesis (43,44). To separate the possible effects of glucopenia at the level of the central nervous system from direct effects of glucopenia on the liver Connolly et al (45) conducted further studies in the conscious dog model.…”

Section: Autoregulation In Response To Hypoglycemiamentioning

confidence: 99%

Autoregulation of hepatic glucose production

Moore

Connolly

Cherrington

1998

European Journal of Endocrinology

104

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In vitro evidence indicates that the liver responds directly to changes in circulating glucose concentrations with reciprocal changes in glucose production and that this autoregulation plays a role in maintenance of normoglycemia. Under in vivo conditions it is dif®cult to separate the effects of glucose on neural regulation mediated by the central nervous system from its direct effect on the liver. Nevertheless, it is clear that nonhormonal mechanisms can cause signi®cant changes in net hepatic glucose balance. In response to hyperglycemia, net hepatic glucose output can be decreased by as much as 60±90% by nonhormonal mechanisms. Under conditions in which hepatic glycogen stores are high (i.e. the overnight-fasted state), a decrease in the glycogenolytic rate and an increase in the rate of glucose cycling within the liver appear to be the explanation for the decrease in hepatic glucose output seen in response to hyperglycemia. During more prolonged fasting, when glycogen levels are reduced, a decrease in gluconeogenesis may occur as a part of the nonhormonal response to hyperglycemia.A substantial role for hepatic autoregulation in the response to insulin-induced hypoglycemia is most clearly evident in severe hypoglycemia (#2.8 mmol/l). The nonhormonal response to hypoglycemia apparently involves enhancement of both gluconeogenesis and glycogenolysis and is capable of supplying enough glucose to meet at least half of the requirement of the brain. The nonhormonal response can include neural signaling, as well as autoregulation. However, even in the absence of the ability to secrete counterregulatory hormones (glucocorticoids, catecholamines, and glucagon), dogs with denervated livers (to interrupt neural pathways between the liver and brain) were able to respond to hypoglycemia with increases in net hepatic glucose output. Thus, even though the endocrine system provides the primary response to changes in glycemia, autoregulation plays an important adjunctive role. European Journal of Endocrinology 138 240±248

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Reciprocal Influences of the Ventromedial and Lateral Hypothalamic Nuclei on Blood Glucose Level and Liver Glycogen Content

Cited by 232 publications

References 3 publications

The Effects of Bilateral Destruction of the Hypothalanhc Feeding Centre on Fastinc Blood Sugar, Glucose Absorption and Glucose Tolerance in the Rat

The Effects of Bilateral Destruction of the Hypothalanhc Feeding Centre on Fastinc Blood Sugar, Glucose Absorption and Glucose Tolerance in the Rat

Potential Role for AMP-Activated Protein Kinase in Hypoglycemia Sensing in the Ventromedial Hypothalamus

Autoregulation of hepatic glucose production

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