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2005
Academisch Ziekenhuis
Maastricht, afd. Inwendige Geneeskunde,
Postbus 5800, 6202 AZ, Maastricht.
The increased risk of fractures
in elderly people is due not only to a decrease
in bone mass and bone quality but also to
an increased risk of falling. The increased
risk of falling is partly a consequence
of muscular weakness caused by a decrease
in both muscular mass and strength (sarcopenia),
in which the hormonal changes that are typical
of aging play a pivotal role, as well as
of malnutrition, in particular a deficiency
of protein, amino acids, calcium and vitamin
D. Measures that limit the risk of falling
and fractures due to muscular weakness consist
mainly of adequate nutrition, extra calcium
and vitamin D, reduction of the factors
that increase the risk of falling, weight-bearing
exercise to strengthen the muscles and the
use of hip protectors. Hormonal suppletion
has not yet been shown to have a favourable
effect, whereas the disadvantages appear
to be substantial.
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Department of Medicine,
Umea University Hospital, S-901 85 Umea, Sweden.
OBJECTIVE: To evaluate
the interplay among abdominal adipose tissue
distribution, the cortisol axis, the autonomic
nervous system, and insulin resistance.
RESEARCH METHODS AND PROCEDURES: Two age-,
sex-, and BMI-matched groups were studied.
Fifteen subjects were first-degree relatives
of patients with type 2 diabetes (R), and
15 had no family history of diabetes (controls,
C). A hyperinsulinemic euglycemic clamp,
cortisol measurements, and analysis of heart
rate variability (HRV) were performed. Computed
tomography was performed in a subgroup (n
= 9 + 9) to determine abdominal adipose
tissue distribution. RESULTS: R tended to
be less insulin-sensitive than C (M value
9.2 +/- 1.0 vs 10.3 +/- 0.7 mg/kg per minute,
not significant). Stimulation with tetracosactin
or corticotropin releasing hormone yielded
lower peak serum cortisol levels in R (p
= 0.03 and p = 0.06, respectively). The
amount of visceral abdominal fat (VAT) tended
to be greater in R. In all subjects, VAT
was negatively correlated to insulin sensitivity
(r = -0.93, p < 0.001). There was a positive
association between VAT and resting heart
rate (r = 0.70, p = 0.003) and sympathetic/parasympathetic
ratio in HRV assessment after tilt (r =
0.53, p = 0.03). Subcutaneous abdominal
tissue was not associated with insulin sensitivity
or any of the hormonal or HRV assessments.
DISCUSSION: Subjects genetically predisposed
for type 2 diabetes had a tendency toward
a larger amount of VAT and to lower insulin
sensitivity compared with control subjects.
The amount of visceral fat was strongly
associated with insulin resistance and signs
of a high ratio of sympathetic vs. parasympathetic
reactivity. A large amount of visceral fat
may act in concert with sympathetic/parasympathetic
imbalance to promote the development of
insulin resistance, and this may be partly
independent of genetic background.
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2004
Laboratory of Cell
Biology, Institute of Life Science, Universite
Catholique de Louvain, Louvain-la-Neuve
B 1348, Belgium.
BACKGROUND: There is evidence
that malnutrition in early life induces
a growth retardation leading, in adult life,
to manifest components of the metabolic
syndrome. However, the impact on obesity
seems less clearly established. OBJECTIVE:
To review the effects of foetal and postnatal
malnutrition on the programming of obesity
in the context of the metabolic syndrome,
as well as the link between central obesity
and cardiovascular diseases. METHODS: Included
in the review were recent papers exploring
the mechanisms linking maternal nutrition
with impaired foetal growth and later obesity,
cardiovascular disease, hypertension and
diabetes in humans and animals. RESULTS:
The programming of obesity during foetal
and early postnatal life depends of the
timing of maternal malnutrition as well
as the postnatal environment. Obesity arises
principally in offspring submitted to malnutrition
during early stages of gestation and which
presented early catch-up growth. The programming
may involve the dysregulation of appetite
control or the hormonal environment leading
to a context favourable to obesity development
(hypersecretion of corticosteroids, hyperinsulinaemia
and hyperleptinaemia and anomalies in the
IGF axis). Adipose tissue secretes actively
several factors implicated in inflammation,
blood pressure, coagulation and fibrinolysis.
The programmed development of intra-abdominal
obesity after early growth restriction may
thus favour higher prevalence of hypertension
and cardiovascular diseases. CONCLUSIONS:
Abdominal obesity appears in malnourished
offspring and is aggravated by early catch-up
growth. Higher rates of intra-abdominal
obesity observed after growth restriction
may participate to hypertension and create
atherothrombotic conditions leading to the
development of cardiovascular diseases.
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1995
Department of Physiology,
University of Texas Health Science Center,
San Antonio 78284-7756, USA.
Neuroendocrine changes
contribute to female reproductive aging,
but changes in other tissues also play a
role. In C57BL/6J mice, neuroendocrine changes
contribute to estrous cycle lengthening
and reduced plasma estradiol levels, but
the midlife loss of cyclicity is mainly
due to ovarian failure. Hypothalamic estrogen
receptor dynamics and estrogenic modulation
of gene expression are altered in middle-aged
cycling mice. Although insufficient to arrest
cyclicity, these neuroendocrine changes
may contribute to other reproductive aging
phenomena, such as altered gonadotropin
secretion and lengthened estrous cycles.
In women, the loss of ovarian oocytes, the
cause of menopause, accelerates in the decade
before menopause. Accelerated oocyte loss
may in turn be caused by a selective elevation
of plasma follicle stimulating hormone,
and neuroendocrine involvement may thus
be implicated in menopausal oocyte loss.
Chronic calorie restriction retards both
neural and ovarian reproductive aging processes,
as well as age-related change in many other
physiological systems. The diverse effects
of food restriction raises the possibility
of an underlying coordinated regulatory
response of the organism to reduced caloric
intake, possibly effected through alterations
of neural and/or endocrine signalling. We
are therefore attempting to identify neuroendocrine
changes that may coordinate the life prolonging
response of animals to food restriction.
Our initial focus is on the glucocorticoid
system. Food restricted rats exhibit daily
periods of hyperadrenocorticism, manifest
as elevated free corticosterone during the
diurnal peak. We hypothesize that this hyperadrenocortical
state potentiates cellular and organismic
homeostasis throughout life in a manner
similar to that achieved during acute stress,
thereby retarding aging processes and extending
life span.
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1989
University of Sydney,
Australia.
Hormones can promote or
inhibit aging depending on the experimental
conditions employed. The aging effects of
hormones are demonstrated by reducing hormone
secretion by hypophysectomy or chronic underfeeding
in young or mature rats. These result in
depressing whole body metabolism, growth,
body temperature and blood glucose levels,
heart rate and vital capacity, gene expression,
etc., but delaying aging of tissues, suppressing
development of pathology and tumors, and,
in underfed rats, prolonging life span.
The anti-aging effects of hormones are demonstrated
by elevating hormone levels in old rats
whose hormones have declined as a result
of dysfunctions that develop in the neuroendocrine
system with age. An increase of hormones
in these rats promotes gene expression,
elevates protein synthesis, and enhances
metabolism, growth, and function of stimulated
organs and tissues.
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