Daily variation of food-induced changes in blood glucose and insulin in the rat and the control by the suprachiasmatic nucleus and the vagus nerve

Strubbe, J.H.; Prins, A.J.A.; Bruggink, J.E.; Steffens, A.B.

doi:10.1016/0165-1838(87)90108-1

Cited by 45 publications

(38 citation statements)

References 18 publications

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“…When food presentation was restricted to the light phase (9:00-15:00), the circa dian pattern of blood glucose was shifted, depending on the time of food intake. These results agreed with the previous reports (15,16). Figure 5 shows the negative correlation between the sur vival time in mice exposed to normobaric hypoxic gas and blood glucose.…”

Section: Resultssupporting

confidence: 83%

Circadian Rhythm in the Cerebral Resistance to Hypoxia in Mice

Masukawa

Tochino

1993

Japanese Journal of Pharmacology

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ABSTRACT-The cerebral resistance to hypoxia in mice was investigated by measuring the survival time under both hypobaric and normobaric hypoxic conditions. In the ad libitum fed mice, there was a circadian variation in the survival time that was longer during the light period than during the dark period under hypobaric hypoxic conditions. The survival time under normobaric hypoxic conditions also exhibited a similar circadian variation in the ad libitum fed mice, whereas the rhythm of the survival time was completely reversed by the restriction of food presentation (9:00-15:00). These findings suggest that there is a circadian rhythm in the cerebral resistance of mice to hypoxia, which can be shifted by the time of food presentation. Furthermore, regression analyses revealed a negative correlation between the survival time of mice exposed to hypoxia and body temperature, and blood glucose levels. These indicate that the cerebral resistance to hypoxia was intimately associated with body temperature and blood glucose that both show a circadian rhythm in mice.

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Section: Resultssupporting

confidence: 83%

Circadian Rhythm in the Cerebral Resistance to Hypoxia in Mice

Masukawa

Tochino

1993

Japanese Journal of Pharmacology

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“…Therefore, data from our regular-fed animals and the results of Boden et al (18) clearly show that a rhythm in insulin release cannot be the primary cause of the diurnal leptin rhythm. As the six meals per day feeding schedule does not result in increased body weight or increased plasma insulin levels (27,30,37), it is not clear what causes the increased plasma leptin levels in our regular-fed group. In fact, as these animals are slightly food-deprived, a lowering of plasma leptin levels would be expected.…”

Section: Discussionmentioning

confidence: 76%

The Suprachiasmatic Nucleus Generates the Diurnal Changes in Plasma Leptin Levels

Kalsbeek¹,

Fliers²,

Romijn

et al. 2001

Endocrinology

227

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At present it is not clear which factors are responsible for the diurnal pattern of plasma leptin levels, although the timing of food intake and circulating hormones such as glucocorticoids and insulin have both been proposed as independent determinants. In this study we show that ablation of the biological clock by thermal lesions of the hypothalamic suprachiasmatic nucleus (SCN) completely eliminates the diurnal pattern of plasma leptin levels. By contrast, removal of the diurnal corticosterone signal by adrenalectomy and corticosterone replacement did not affect diurnal plasma leptin levels. More importantly, removal of the nocturnal feeding signal by submitting the animals to a regular feeding schedule of six meals per day did not abolish the diurnal plasma leptin levels. However, both SCN lesions and the regular feeding schedule did cause an increase in the 24-h mean plasma leptin levels. As neither rhythmic feeding, insulin, or corticosterone signals can completely explain the diurnal plasma leptin rhythm, we conclude that biological clock control of the sympathetic input to the adipocyte is essential for regulation of the daily rhythm in leptin release.

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“…In addition to the close control of blood glucose levels, the secretion of insulin is in part regulated by the vagus nerve. Activation of the parasympathetic nervous system can stimulate the secretion of insulin (22,44) and enhance the insulin secretory response to glucose (37). It has been suggested that central administration of NPY may act directly on the nucleus of solitary tract, which may mediate the direct link to the pancreas via a vagal pathway to enhance insulin secretion (10).…”

Section: Discussionmentioning

confidence: 99%

Selective activation of central NPY Y1 vs. Y5 receptor elicits hyperinsulinemia via distinct mechanisms

Gao¹,

Ghibaudi²,

Hwa³

2004

American Journal of Physiology-Endocrinology and Metabolism

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Recent evidence has suggested that the Y1 and Y5 receptor subtypes may both mediate NPYstimulated feeding. The present study attempts to further characterize the role of central NPY receptor subtypes involved in hyperinsulinemia. NPY and peptide analogs of NPY that selectively activated the NPY Y1 or Y5 receptor subtype induced feeding and hyperinsulinemia in satiated Long Evans rats, whereas NPY analogs that selectively activated the NPY Y2 or Y4 receptor subtype did not. To determine whether NPY-induced hyperinsulinemia is secondary to its hyperphagic effect, we compared the plasma insulin levels in the presence and absence of food after a 1-min central infusion of NPY and its analogs at 15, 60, and 120 min postinfusion. Our data suggest that selective activation of central NPY Y1 receptor subtype induced hyperinsulinemia independent of food ingestion, whereas the NPY Y5 receptor-induced hyperinsulinemia was dependent on food ingestion. Central administration of the selective Y1 receptor agonist D-Arg 25 NPY eventually decreased plasma glucose levels 2 h postinfusion in Long Evans rats. neuropeptide Y; insulin; glucagon; glucose; food and brain NEUROPEPTIDE Y (NPY) is a 36-amino-acid neurotransmitter that is highly concentrated in the hypothalamus (8). In the hypothalamus, NPY is synthesized in the arcuate nucleus, which projects into the paraventricular nuclei and the dorsomedial nuclei to release NPY (1). In the periphery, NPY is colocalized with norepinephrine in sympathetic nerve endings (32). A variety of studies have linked NPY to physiological processes related to feeding behavior, energy homeostasis, neuroendocrine interactions, cardiovascular regulation, and emotional integration (9,12,15,19,35).NPY is a member of the pancreatic polypeptide family, which elicits a wide variety of physiological effects via the activation of G protein-coupled receptors (Y1, Y2, Y4, Y5, and y6) (5). NPY receptor subtypes are all present in the hypothalamus (30) and have been suggested to play a role in modulating food intake and energy expenditure (4, 16). However, whether one of the receptor subtypes is the most likely candidate for central NPY-induced hyperinsulinemia has not been clearly elucidated. Chronic and acute administration of NPY intracerebroventricularly (icv) elicits hyperinsulinemia in a variety of species (10,11,20,26,39,47). The insulinemic response to hypothalamic or icv NPY is largely dependent on the consumption of food (20, 24, 26) but also occurs when eating is prevented (24, 39). It has been suggested that central administration of NPY could stimulate insulin release through modulation of the autonomic nervous system (38), because NPY activates the parasympathetic nervous system (14) and causes increased firing of the vagus nerve (11, 25). The resulting hyperinsulinemia could contribute substantially to the anabolic effects of NPY (33).The aim of this study was to evaluate the effects of selective NPY Y1, Y2, Y4, and Y5 receptor agonists on plasma insulin, glucose, and glucagon levels in the presen...

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Daily variation of food-induced changes in blood glucose and insulin in the rat and the control by the suprachiasmatic nucleus and the vagus nerve

Cited by 45 publications

References 18 publications

Circadian Rhythm in the Cerebral Resistance to Hypoxia in Mice

Circadian Rhythm in the Cerebral Resistance to Hypoxia in Mice

The Suprachiasmatic Nucleus Generates the Diurnal Changes in Plasma Leptin Levels

Selective activation of central NPY Y1 vs. Y5 receptor elicits hyperinsulinemia via distinct mechanisms

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