Hyperglycaemia as an inducer as well as a consequence of impaired islet cell function and insulin resistance: implications for the management of diabetes

Research output: Contribution to journalArticle

433 Citations (Scopus)

Abstract

It is postulated that hyperglycaemia influences the natural history of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia, even when mild, can attenuate the secretory response of pancreatic β and α cells to increments in glucose and can impair insulin-mediated glucose transport, thus impeding its own correction and initiating a cycle of progressive self-exacerbation and metabolic deterioration. Both reduced islet function and insulin action may be the consequence of a generalized down-regulation and/or occupation of glucose transporters by hyperglycaemia so that the islets respond less to further increments in glycaemia. The postulated hyperglycaemic cycle can be initiated by any environmental perturbation that increases insulin demand in previously normoglycaemic patients in whom insulin secretion has already reached a maximum level of compensation for peripheral insulin resistance (as in obese pre-Type 2 diabetes) or for a reduced β-cell mass (as in pre-Type 1 diabetes). Elimination of hyperglycaemia by any means can halt this cycle of progressive metabolic deterioration and may restore transiently metabolic recompensation both in Type 1 and Type 2 diabetes. There is experimental evidence that long-standing severe hyperglycaemia may irreversibly damage β cells.

Original languageEnglish (US)
Pages (from-to)119-121
Number of pages3
JournalDiabetologia
Volume28
Issue number3
DOIs
StatePublished - Mar 1985

Fingerprint

Islets of Langerhans
Hyperglycemia
Insulin Resistance
Insulin
Type 2 Diabetes Mellitus
Glucose
Facilitative Glucose Transport Proteins
Natural History
Type 1 Diabetes Mellitus
Occupations
Vascular Resistance
Down-Regulation

Keywords

  • diabetic remissions
  • glucagon
  • Hyperglycaemia
  • insulin
  • islet cell function
  • Type 1 diabetes
  • Type 2 diabetes

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

@article{844460be55344af4a37d5133b2e9d6d7,
title = "Hyperglycaemia as an inducer as well as a consequence of impaired islet cell function and insulin resistance: implications for the management of diabetes",
abstract = "It is postulated that hyperglycaemia influences the natural history of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia, even when mild, can attenuate the secretory response of pancreatic β and α cells to increments in glucose and can impair insulin-mediated glucose transport, thus impeding its own correction and initiating a cycle of progressive self-exacerbation and metabolic deterioration. Both reduced islet function and insulin action may be the consequence of a generalized down-regulation and/or occupation of glucose transporters by hyperglycaemia so that the islets respond less to further increments in glycaemia. The postulated hyperglycaemic cycle can be initiated by any environmental perturbation that increases insulin demand in previously normoglycaemic patients in whom insulin secretion has already reached a maximum level of compensation for peripheral insulin resistance (as in obese pre-Type 2 diabetes) or for a reduced β-cell mass (as in pre-Type 1 diabetes). Elimination of hyperglycaemia by any means can halt this cycle of progressive metabolic deterioration and may restore transiently metabolic recompensation both in Type 1 and Type 2 diabetes. There is experimental evidence that long-standing severe hyperglycaemia may irreversibly damage β cells.",
keywords = "diabetic remissions, glucagon, Hyperglycaemia, insulin, islet cell function, Type 1 diabetes, Type 2 diabetes",
author = "Unger, {R. H.} and S. Grundy",
year = "1985",
month = "3",
doi = "10.1007/BF00273856",
language = "English (US)",
volume = "28",
pages = "119--121",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer Verlag",
number = "3",

}

TY - JOUR

T1 - Hyperglycaemia as an inducer as well as a consequence of impaired islet cell function and insulin resistance

T2 - implications for the management of diabetes

AU - Unger, R. H.

AU - Grundy, S.

PY - 1985/3

Y1 - 1985/3

N2 - It is postulated that hyperglycaemia influences the natural history of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia, even when mild, can attenuate the secretory response of pancreatic β and α cells to increments in glucose and can impair insulin-mediated glucose transport, thus impeding its own correction and initiating a cycle of progressive self-exacerbation and metabolic deterioration. Both reduced islet function and insulin action may be the consequence of a generalized down-regulation and/or occupation of glucose transporters by hyperglycaemia so that the islets respond less to further increments in glycaemia. The postulated hyperglycaemic cycle can be initiated by any environmental perturbation that increases insulin demand in previously normoglycaemic patients in whom insulin secretion has already reached a maximum level of compensation for peripheral insulin resistance (as in obese pre-Type 2 diabetes) or for a reduced β-cell mass (as in pre-Type 1 diabetes). Elimination of hyperglycaemia by any means can halt this cycle of progressive metabolic deterioration and may restore transiently metabolic recompensation both in Type 1 and Type 2 diabetes. There is experimental evidence that long-standing severe hyperglycaemia may irreversibly damage β cells.

AB - It is postulated that hyperglycaemia influences the natural history of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia, even when mild, can attenuate the secretory response of pancreatic β and α cells to increments in glucose and can impair insulin-mediated glucose transport, thus impeding its own correction and initiating a cycle of progressive self-exacerbation and metabolic deterioration. Both reduced islet function and insulin action may be the consequence of a generalized down-regulation and/or occupation of glucose transporters by hyperglycaemia so that the islets respond less to further increments in glycaemia. The postulated hyperglycaemic cycle can be initiated by any environmental perturbation that increases insulin demand in previously normoglycaemic patients in whom insulin secretion has already reached a maximum level of compensation for peripheral insulin resistance (as in obese pre-Type 2 diabetes) or for a reduced β-cell mass (as in pre-Type 1 diabetes). Elimination of hyperglycaemia by any means can halt this cycle of progressive metabolic deterioration and may restore transiently metabolic recompensation both in Type 1 and Type 2 diabetes. There is experimental evidence that long-standing severe hyperglycaemia may irreversibly damage β cells.

KW - diabetic remissions

KW - glucagon

KW - Hyperglycaemia

KW - insulin

KW - islet cell function

KW - Type 1 diabetes

KW - Type 2 diabetes

UR - http://www.scopus.com/inward/record.url?scp=0021961644&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021961644&partnerID=8YFLogxK

U2 - 10.1007/BF00273856

DO - 10.1007/BF00273856

M3 - Article

C2 - 3888754

AN - SCOPUS:0021961644

VL - 28

SP - 119

EP - 121

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 3

ER -