Part of this work was presented at the 13th Congress of the International Diabetes Federation, Sydney, Australia 1988 and the British Geriatric Society Spring Meeting, Manchester, UK, 1989.
Peripheral and hepatic insulin sensitivity in healthy elderly human subjects
Article first published online: 20 MAR 2008
European Journal of Clinical Investigation
Volume 21, Issue 1, pages 13–21, February 1991
How to Cite
BROUGHTON, D.L., JAMES, O.W.F., ALBERTI, K.G.M.M. and TAYLOR, R. (1991), Peripheral and hepatic insulin sensitivity in healthy elderly human subjects. European Journal of Clinical Investigation, 21: 13–21. doi: 10.1111/j.1365-2362.1991.tb01352.x
- Issue published online: 20 MAR 2008
- Article first published online: 20 MAR 2008
- Received 16 February 1990 and in revised form 20 August 1990
- Body weight;
- exercise test;
- glucose tolerance test;
- insulin resistance
Abstract. Insulin resistance has been reported in normal ageing but discrepancies between such studies may be related to compounding factors such as body composition and exercise patterns. We employed a two-step hyperinsulinaemic euglycaemic clamp to assess peripheral and hepatic tissue insulin sensitivity and glucose recycling in 13 elderly (E) and 14 young (Y) healthy subjects controlling for the above factors. There was no difference in basal hepatic glucose production (E: 2±36 ± 0±06, Y: 2±47 ± 0±1 mg kg–1 min–1; P= 0±4). At step 1 (insulin infusion 15mUkg–1 h–1) glucose turnover was similar (E: 2±65 ± 0±13, Y: 2±88 ± 0±22 mg kg–1 min–1; P= 0±4) but hepatic glucose production was lower in the elderly group (0±20 ± 0±16 vs 0±64 ± 0±10 mg kg–1 min–1; P= 0±03). At step 2 (insulin infusion 50 mU kg–1 h–1) glucose turnover was similar (E: 7±60 ± 0±24, Y: 8±05 ± 0±34 mg kg–1 min–1; P= 0±3) and hepatic glucose production was equal but negative (E: –1±35 ± 0±18, Y: -1±34 ± 0±22 mg kg–1 min–1; P= 0±9). Glucose recycling did not differ between the groups at any stage. Similar serum insulin levels were achieved in both groups at each step. Decreased glucose tolerance was confirmed in E with a higher 2 h blood glucose after an OGTT (5±3 ± 0±4 vs 4±1 ± 0±3 mmol l–1; P= 0±03) but incremental insulin response was similar (E: 3236 ± 289, Y: 3586 ± 463 mU l–1 min–1; P= 0±5). We conclude that changes in hepatic tissue insulin sensitivity do not cause the deterioration in glucose tolerance observed with age. A small reduction in both peripheral tissue insulin sensitivity and late insulin secretion may be responsible.