Somatopause and Elderly GHD – Similarities and Differences
Horm Res 2003;60(suppl 1):102–104
DOI: 10.1159/000071233
Effects of Ageing on Insulin Secretion
and Action
Niels Møller Lars Gormsen Jens Fuglsang Jakob Gjedsted
Medical Department M (Endocrinology and Diabetes) and Institute of Experimental Research, University of Aarhus,
Aarhus, Denmark
Dr. N. Møller
Medical Department M (Endocrinology and Diabetes) and
Institute of Experimental Research, University of Aarhus
DK–8000 Aarhus (Denmark)
Tel. +45 89 49 21 65, Fax +45 89 49 20 10, E-Mail nielsem@dadlnet.dk
ABC
Fax + 41 61 306 12 34
E-Mail karger@karger.ch
www.karger.com
© 2003 S. Karger AG, Basel
0301–0163/03/0607–0102$19.50/0
Accessible online at:
www.karger.com/hre
Key Words
Insulin W Insulin resistance W Ageing W Type 2 diabetes
mellitus W Insulin secretion
Abstract
One of the many conditions associated with ageing is
type 2 diabetes mellitus, the prevalence of which in-
creases from 20–30 years of age onwards. In many
cases, type 2 diabetes mellitus is caused by the combina-
tion of insulin resistance and poor insulin secretion. Insu-
lin resistance is also a risk factor associated with other
disorders, in particular cardiovascular disease. Physio-
logical changes associated with ageing, such as changes
in body composition, decreased physical fitness,
changes in hormones, and the secondary effects of high
levels of free fatty acids and glucose, may also contribute
to the impairment of insulin secretion and action. In this
review, the effects of ageing on the secretion and action
of insulin will be highlighted.
Copyright © 2003 S. Karger AG, Basel
Introduction
Propelled by the ever-growing world population and
the continual rise in life expectancy, ageing is becoming a
more frequent and lengthy ‘condition’. The process of
ageing is characterized by a number of physiological and
pathophysiological alterations, which, in many cases, can
lead to impaired physical performance and increased
morbidity and mortality. Type 2 diabetes mellitus (non-
insulin dependent) is such an example. Data from the
Framingham Study show unequivocally that the inci-
dence of type 2 diabetes rises steeply with age, at an
almost exponential rate, from the age of 20–30 years
onwards [1]. Prevalence rates show a similar pattern from
1% between 30 and 40 years of age to more than 15%
above 80 years of age. These observations were published
in 1986 and both the incidence and prevalence rates are
continuously rising because of increased life expectancy,
increased prevalence and magnitude of obesity, and poor
inclination to physical activity. The picture becomes even
more alarming when one considers pre-diabetic states.
Type 2 diabetes is, in most cases, caused by a combination
of defective insulin secretion and insulin resistance. At
present, there is accumulating evidence that insulin resis-
tance is a substantial risk factor for cardiovascular disease
[2, 3]. The terms ‘metabolic syndrome’, ‘insulin resistance
syndrome’, ‘syndrome X’, ‘dysmetabolic syndrome’ and
others have been proposed to represent the clustering of
insulin resistance, obesity, hypertension, dyslipidaemia
and hypercoagulability. According to World Health Orga-
nization criteria, the metabolic syndrome is defined as the
coexistence of insulin resistance and two out of the fol-
lowing four conditions: (1) obesity, (2) dyslipidaemia,
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