Pancreatic Polypeptide

Lonovics, János

doi:10.1001/archsurg.1981.01380220010002

Cited by 100 publications

(47 citation statements)

References 94 publications

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“…The definite increase of insulin deserves emphasis because previous studies have been inconclusive (25). The failure of glucagon and pancreatic polypeptide to respond is of interest because both increase during hypoglycemic stress (26,27) and because their clear absence of response helps to validate the positive results for other variables. The definite responses of these ten variables to phobic anxiety increase confidence in our previous reports, based on a similar method, that plasma TSH and prolactin are not changed by phobic anxiety (15,16).…”

Section: Discussionmentioning

confidence: 99%

“…Could anxiety-induced changes in glucagon and pancreatic polypeptide have been missed because their half-lives in plasma are only about 5 min (26,27)? Although single brief peaks might escape detection, repeated peaks would have been reflected in the analysis, as they were for the catecholamines which have even shorter half-lives (33).…”

Section: Discussionmentioning

confidence: 99%

“…The influence of stress on insulin has been uncertain (25) but of obvious importance for understanding glucose regulation. Glucagon and pancreatic polypeptide are the other two islet cell hormones whose plasma levels mainly reflect pancreatic secretion (26,27). Both increase during hypoglycemia, and glucagon release might be adaptive during stress because it induces glycogenolysis and gluconeogenesis (26,27).…”

Section: Introductionmentioning

confidence: 99%

“…Glucagon and pancreatic polypeptide are the other two islet cell hormones whose plasma levels mainly reflect pancreatic secretion (26,27). Both increase during hypoglycemia, and glucagon release might be adaptive during stress because it induces glycogenolysis and gluconeogenesis (26,27). Repeated simultaneous measurements of these 12 variables during periods of rest and anxiety make possible a detailed and coordinated view of the responses to psychologic stress.…”

Section: Introductionmentioning

confidence: 99%

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Endocrine and cardiovascular responses during phobic anxiety.

Nesse

Curtis²,

Thyer³

et al. 1985

Psychosomatic Medicine

168

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In vivo exposure therapy for phobias is uniquely suited for controlled studies of endocrine and physiologic responses during psychologic stress. In this study, exposure therapy induced significant increases in subjective anxiety, pulse, blood pressure, plasma norepinephrine, epinephrine, insulin, cortisol, and growth hormone, but did not change plasma glucagon or pancreatic polypeptide. Although the subjective and behavioral manifestations of anxiety were consistent and intense, the magnitude, consistency, timing, and concordance of endocrine and cardiovascular responses showed considerable variation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Endocrine and cardiovascular responses during phobic anxiety.

Nesse

Curtis²,

Thyer³

et al. 1985

Psychosomatic Medicine

168

View full text Add to dashboard Cite

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“…Pancreatic polypeptide (PP) is a hormone that arises from both the PP-cells of the islets of Langerhans and the acinar cells of the pancreas [127]. The secretion of this hormone is regulated by vagal cholinergic mechanisms in response to food intake and plasma glucose [128].…”

Section: Pancreatic Polypeptidementioning

confidence: 99%

Hepatic Steatosis in Type 1 Diabetes

Regnell

Lernmark

2011

Rev Diabet Stud

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■ AbstractIslet autoimmunity in type 1 diabetes results in the loss of the pancreatic β-cells. The consequences of insulin deficiency in the portal vein for liver fat are poorly understood. Under normal conditions, the portal vein provides 75% of the liver blood supply. Recent studies suggest that non-alcoholic fatty liver disease (NAFLD) may be more common in type 1 diabetes than previously thought, and may serve as an independent risk marker for some chronic diabetic complications. The pathogenesis of NAFLD remains obscure, but it has been hypothesized that hepatic fat accumulation in type 1 diabetes may be due to lipoprotein abnormalities, hyperglycemia-induced activation of the transcription factors carbohydrate response element-binding protein (ChREBP) and sterol regulatory element-binding protein 1c (SREBP-1c), upregulation of glucose transporter 2 (GLUT2) with subsequent intrahepatic fat synthesis, or a combination of these mechanisms. Novel approaches to non-invasive determinations of liver fat may clarify the consequences for liver metabolism when the pancreas has ceased producing insulin. This article aims to review the factors potentially contributing to hepatic steatosis in type 1 diabetes, and to assess the feasibility of using liver fat as a prognostic and/or diagnostic marker for the disease. It provides a background and a case for possible future studies in the field.

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