Extrapancreatic Glucagon and Its Regulation

Lefèbvre, Pierre; Luyckx, A

doi:10.1007/978-3-642-69019-8_11

Cited by 7 publications

(2 citation statements)

References 58 publications

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“…We demonstrated a lack of glucagon responsivity to arginine in a subset of pancreatectomized dogs, which implies that the glucagon responses we observed in transplanted dogs were secreted from a-cells in pancreatic islets and not from cells of the gastric fundus. This is consistent with previous reports that gastric glucagon is sensitive to inhibition by insulin (25,26) and that gastric glucagon is unresponsive to hypoglycemia (27,28). Basal pancreatic polypeptide levels were low in both of our transplanted groups of dogs, compared with the control dogs, and there were no significant increments in pancreatic polypeptide in response to insulin-induced hypoglycemia following autotransplantation in either the intrahepatic or intraperitoneal site.…”

Section: Discussionsupporting

confidence: 93%

The Defective Glucagon Response From Transplanted Intrahepatic Pancreatic Islets During Hypoglycemia Is Transplantation Site–Determined

et al. 1997

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The optimal site for pancreatic islet cell transplantation is presently unclear, although the liver has been the most commonly used. However, glucagon secretion from islets that have been autotransplanted in liver has been reported to be unresponsive to hypoglycemia yet responsive to arginine. To determine whether this selective glucagon secretory defect is related to the intrahepatic site of islet implantation or to the process of transplantation per se, we studied counterregulatory responses to hypoglycemia in dogs with pancreatic islet autotransplantation in the hepatic parenchyma (the intrahepatic [IH] group, n = 9) or the peritoneal cavity (the intraperitoneal [IP] group, n = 9), following total pancreatectomy, and compared them with the responses in normal controls (n = 10). Dogs were subjected to a hypoglycemic hyperinsulinemic (5 mU x kg-1 x min-1) clamp for 90 min under general anesthesia. Arterial glucose concentrations were clamped at 2.7 mmol/l for the final 45 min of the clamp. Immediately following the clamp, glucagon responses to IV arginine (5 g) were also assessed. During hypoglycemia, glucagon responses in the IH group (maximal incremental glucagon = 33 +/- 21 ng/l; glucagon area under curve [AUC] = 713 +/- 1,022 ng x l-1 x min-1) were significantly lower than either the IP (maximal incremental glucagon = 92 +/- 32 ng/l; glucagon AUC = 4,090 +/- 1,600 ng x l-1 x min-1) or control (maximal incremental glucagon = 154 +/- 71 ng/l; glucagon AUC = 6,943 +/- 2,842 ng x l-1 x min-1) group (IH vs. IP group, P < 0.05; control vs. IH group, P < 0.01). Glucagon responses in the IP group did not differ significantly from the control group. Epinephrine responses to hypoglycemia were similar in all groups, whereas neither of the transplanted groups (IH and IP) had pancreatic polypeptide responses. There was a prompt rise in plasma glucagon after intravenous arginine in all groups. These data indicate that glucagon unresponsiveness to hypoglycemia is specific to intrahepatically transplanted islets, rendering the liver a disadvantageous site for optimal alpha-cell function.

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Section: Discussionsupporting

confidence: 93%

The Defective Glucagon Response From Transplanted Intrahepatic Pancreatic Islets During Hypoglycemia Is Transplantation Site–Determined

et al. 1997

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“…This failure of glucagon levels to fall after two-thirds pancreatectomy in dogs is not surprising, because gastric a-cells are a major source of circulating pancreatic-type glucagon in the dog (27). Such compensation was very effective because neither FPG nor HbA lc rose despite normal food intake and maintenance of body weight.…”

Section: Glucosementioning

confidence: 99%

Reduction of Glycemic Potentiation: Sensitive Indicator of β-Cell Loss in Partially Pancreatectomized Dogs

et al. 1988

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To determine which test of islet function is the most sensitive indicator of subclinical beta-cell loss, we studied six conscious dogs before and 1 and 6 wk after removal of the splenic and uncinate lobes [64 +/- 2% pancreatectomy (PX)]. To assess hyperglycemic potentiation, acute insulin secretory responses (AIR) to 5 g i.v. arginine were measured at the fasting plasma glucose (FPG) level after PG was clamped at approximately 250 mg/dl and after PG was clamped at a maximally potentiating level of 550-650 mg/dl. FPG levels were unaffected by PX (112 +/- 4 mg/dl pre-PX vs. 115 +/- 5 mg/dl 6 wk after PX, P NS). Similarly, basal insulin levels remained constant after PX (11 +/- 2 microU/ml pre-PX vs. 11 +/- 1 microU/ml 6 wk after PX, P NS). The AIR to 300 mg/kg i.v. glucose decreased slightly from 42 +/- 9 microU/ml pre-PX to 32 +/- 5 microU/ml 6 wk after PX (P NS), and thus the beta-cell loss was underestimated. In contrast, insulin responses to arginine declined markedly after PX. The AIR to arginine obtained at FPG levels declined from 23 +/- 3 microU/ml pre-PX to 13 +/- 2 microU/ml 6 wk after PX (P = .04). The AIR to arginine obtained at PG levels of approximately 250 mg/dl declined even more, from a pre-PX value of 56 +/- 7 microU/ml to 21 +/- 4 microU/ml 6 wk after PX (P = .02).(ABSTRACT TRUNCATED AT 250 WORDS)

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Gut Glucagon

Bataille¹

1989

Comprehensive Physiology

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Extrapancreatic Glucagon and Its Regulation

Cited by 7 publications

References 58 publications

The Defective Glucagon Response From Transplanted Intrahepatic Pancreatic Islets During Hypoglycemia Is Transplantation Site–Determined

The Defective Glucagon Response From Transplanted Intrahepatic Pancreatic Islets During Hypoglycemia Is Transplantation Site–Determined

Reduction of Glycemic Potentiation: Sensitive Indicator of β-Cell Loss in Partially Pancreatectomized Dogs

Gut Glucagon

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