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 language | English (US) |
|---|---|
| Pages (from-to) | 119-121 |
| Number of pages | 3 |
| Journal | Diabetologia |
| Volume | 28 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1985 |
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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
Hyperglycaemia as an inducer as well as a consequence of impaired islet cell function and insulin resistance : implications for the management of diabetes. / Unger, R. H.; Grundy, S.
In: Diabetologia, Vol. 28, No. 3, 03.1985, p. 119-121.Research output: Contribution to journal › Article
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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 -