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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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