Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats.

Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Research Abstract Details 

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Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Abstract Text:

Huarong Zhou,Tao Zhang,Elizabeth Oseid,Jamie Harmon,Naoko Tonooka,R Paul Robertson,

The intraislet insulin hypothesis has been proposed to explain absent glucagon responses to hypoglycemia. Recently we directly confirmed this hypothesis by restoring glucagon secretion via provision of a pancreatic artery insulin infusion, which was switched off at the time of hypoglycemia in Wistar rats made diabetic by streptozotocin. The current study examined this hypothesis in a model of spontaneous, autoimmune diabetes, the insulin-dependent diabetic BB rat. The insulin switch-off signal restored the defective glucagon responses to hypoglycemia. However, the magnitude of the restored response was markedly less than that observed in control nondiabetic BB rats (4- to 5-month-old diabetic BB rats = 147 +/- 27; 2-month-old nondiabetic BB rats = 1038 +/- 112 pg/ml, peak delta; P < 0.0001). Because time was required for the BB rat to spontaneously develop diabetes, we asked whether the incomplete restoration of the glucagon response might be related to the animals' growth and development. This led us to compare the glucagon response to hypoglycemia in nondiabetic BB and Wistar rats at 2 and 4-5 months of age. We observed age-related deterioration of not only glucose tolerance and insulin sensitivity but also glucagon responses to hypoglycemia in both strains. There was no significant difference between the glucagon responses to hypoglycemia in age-matched nondiabetic BB rats and diabetic BB rats provided with the insulin switch-off signal. We conclude that defective glucagon responses to hypoglycemia in BB rats can be corrected by restoring regulation of alpha-cell function by insulin.

Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Publishing Authors By Initials

H Zhou,T Zhang,E Oseid,J Harmon,N Tonooka,RP Robertson,

For similar animals: chordata: vertebrates: mammals: rodentia: muridae: murinae: rats: rats, wistar research abstracts see: animals: chordata: vertebrates: mammals: rodentia: muridae: murinae: rats: rats, wistar research

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Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Endocrinology

VOLUME: 148

Page Numbers: 2863-9

Journal Abbreviation: Endocrinology

ISSN: 0013-7227

DAY: 8

MONTH: 03

YEAR: 2007

Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 375040

Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Keywords Mesh Terms:

KEYWORDS: Rats, Wistar

MESH TERMS: administration & dosage

Chemical & Substance for Abstract: Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats. Information

Substance Name: Glucagon

Registry Number: 9007-92-5

Grant and Affiliation Information for Reversal of defective glucagon responses to hypoglycemia in insulin-dependent autoimmune diabetic BB rats.

AFFILIATION: Pacific Northwest Research Institute, 720 Broadway, Seattle, WA 98122, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: R01 DK 39994

ACRONYM: DK

MEDLINETA: Endocrinology

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