Interplay of Nutrients and Hormones in the Regulation of Glucagon Release*

Pipeleers, Daniël; SCHUIT, F. C.; Schravendijk, C. F. H. Van; Winkel, M. Van De

doi:10.1210/endo-117-3-817

Cited by 177 publications

(135 citation statements)

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“…From a broader physiologic standpoint, it seems interesting to examine whether comparable coordinate pathways occur in other endocrine cell populations. A similar pattern has been noted in the regulation of pancreatic A cells, in which a synergistic interaction between cell specific nutrient and (neuro)hormonal signals was found to regulate the rate of glucagon release [86][87][88].…”

Section: Synergistic Interaction With Environmental Signalssupporting

confidence: 62%

The biosociology of pancreatic B cells

1987

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Section: Synergistic Interaction With Environmental Signalssupporting

confidence: 62%

The biosociology of pancreatic B cells

1987

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“…It is known that amino acids have stimulatory effects and that FFAs and ketones have inhibitory effects on glucagon secretion from the ␣-cell in the pancreas (22,41,55). As shown in Table 1, blood amino acid concentrations decreased, and plasma NEFA and ketone concentrations increased with the decrement in plasma glucose.…”

Section: Discussionmentioning

confidence: 95%

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

et al. 2001

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The responses of the pancreatic ␣-and ␤-cells to small changes in glucose were examined in overnight-fasted conscious dogs. Each study consisted of an equilibration (-140 to -40 min), a control (-40 to 0 min), and a test period (0 to 180 min), during which BAY R3401 (10 mg/kg), a glycogen phosphorylase inhibitor, was administered orally, either alone to create mild hypoglycemia or with peripheral glucose infusion to maintain euglycemia or create mild hyperglycemia. Drug administration in the hypoglycemic group decreased net hepatic glucose output (NHGO) from 8.9 ± 1.7 (basal) to 6.0 ± 1.7 and 5.8 ± 1.0 µmol · kg -1 · min -1 by 30 and 90 min. As a result, the arterial plasma glucose level decreased from 5.8 ± 0.2 (basal) to 5.2 ± 0.3 and 4.4 ± 0.3 mmol/l by 30 and 90 min, respectively (P < 0.01). Arterial plasma insulin levels and the hepatic portalarterial difference in plasma insulin decreased (P < 0.01) from 78 ± 18 and 90 ± 24 to 24 ± 6 and 12 ± 12 pmol/l over the first 30 min of the test period and decreased to 18 ± 6 and 0 pmol/l by 90 min, respectively. The arterial glucagon levels and the hepatic portal-arterial difference in plasma glucagon increased from 43 ± 5 and 4 ± 2 to 51 ± 5 and 10 ± 5 ng/l by 30 min (P < 0.05) and to 79 ± 16 and 31 ± 15 ng/l by 90 min (P < 0.05), respectively. In euglycemic dogs, the arterial plasma glucose level remained at 5.9 ± 0.1 mmol/l, and the NHGO decreased from 10 ± 0.6 to -3.3 ± 0.6 µmol · kg -1 · min -1 (180 min). The insulin and glucagon levels and the hepatic portal-arterial differences remained constant. In hyperglycemic dogs, the arterial plasma glucose level increased from 5.9 ± 0.2 to 6.2 ± 0.2 mmol/l by 30 min, and the NHGO decreased from 10 ± 1.7 to 0 µmol · kg -1 · min -1 by 30 min. The arterial plasma insulin levels and the hepatic portal-arterial difference in plasma insulin increased from 60 ± 18 and 78 ± 24 to 126 ± 30 and 192 ± 42 pmol/l by 30 min, after which they averaged 138 ± 24 and 282 ± 30 pmol/l, respectively. The arterial plasma glucagon levels and the hepatic portal-arterial difference in plasma glucagon decreased slightly from 41 ± 7 and 4 ± 3 to 34 ± 7 and 3 ± 2 ng/l during the test period. These data show that the ␣-and ␤-cells of the pancreas respond as a coupled unit to very small decreases in the plasma glucose level. Diabetes 50:367-375, 2001 G lucagon secretion increases in response to a decrease in the plasma glucose concentration and decreases in response to a rise in the plasma glucose level. Furthermore, insulin has been postulated to exert a paracrine influence on glucagon secretion when its release is modified in response to changes in the plasma glucose concentration. To date, studies have not provided a complete understanding of the relationship between a decrement in the plasma glucose level and glucagon or insulin secretion, because the insulin level itself has been elevated to decrease the glucose level, and insulin per se can affect not only its own secretion (1), but also the release of other counterregulatory hormones, inclu...

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“…In addition to fatty acids, amino acids are also relevant in the modulation of the a-cell function. Amino acids such as arginine, alanine and glutamine are potent stimulators of glucagon secretion (Pipeleers et al 1985, Kuhara et al 1991, Dumonteil et al 2000. However, a few amino acids such as isoleucine can also inhibit a-cell secretion while leucine has a dual effect: it is a positive stimulus at physiological concentrations but becomes a negative one at elevated levels (15 mM; Leclercq-Meyer et al 1985).…”

Section: Regulation Of Glucagon Secretion By Fatty Acids and Amino Acidsmentioning

confidence: 99%

Physiology of the pancreatic α-cell and glucagon secretion: role in glucose homeostasis and diabetes

Quesada¹,

Tudurí²,

Ripoll³

et al. 2008

Journal of Endocrinology

338

330

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The secretion of glucagon by pancreatic a-cells plays a critical role in the regulation of glycaemia. This hormone counteracts hypoglycaemia and opposes insulin actions by stimulating hepatic glucose synthesis and mobilization, thereby increasing blood glucose concentrations. During the last decade, knowledge of a-cell physiology has greatly improved, especially concerning molecular and cellular mechanisms. In this review, we have addressed recent findings on a-cell physiology and the regulation of ion channels, electrical activity, calcium signals and glucagon release. Our focus in this review has been the multiple control levels that modulate glucagon secretion from glucose and nutrients to paracrine and neural inputs. Additionally, we have described the glucagon actions on glycaemia and energy metabolism, and discussed their involvement in the pathophysiology of diabetes. Finally, some of the present approaches for diabetes therapy related to a-cell function are also discussed in this review. A better understanding of the a-cell physiology is necessary for an integral comprehension of the regulation of glucose homeostasis and the development of diabetes.

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Interplay of Nutrients and Hormones in the Regulation of Glucagon Release*

Cited by 177 publications

References 0 publications

The biosociology of pancreatic B cells

The biosociology of pancreatic B cells

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

Physiology of the pancreatic α-cell and glucagon secretion: role in glucose homeostasis and diabetes

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