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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normative age- and gender-related changes in body composition, serum lipids, testosterone, and insulin-like growth factor (IGF-1) were examined in the Cayo Santiago free-ranging rhesus macaques. In both adult males and females, body weights, crown-rump lengths, and circumference of the limbs were lowest in the oldest group (20+ years of age) as compared with other adult age classes. Body fat, as reflected in subcutaneous fatfold thickness and waist/thigh ratios, were higher in adult females than adult males. This gender dimorphism was first detectable among the 6-9 year old age group. Greatest body fat among females was observed in the 10-14 age group, whereas in males the highest values were observed in the 15-19 age group. Differences in body composition were also observed with respect to reproductive status. Although there were no gender differences in overall cholesterol levels, there were age-related differences between males and females, and only in males were cholesterol values positively related to adiposity. There were no age- or gender-related differences in triglyceride values, but levels were significantly higher in pregnant females in comparison with other reproductive states. Levels of testosterone were not significantly related to any morphometric parameter and values did not decrease significantly with age. Levels of IGF-1 exhibited a significant age-related decrease among adult males, and females had higher levels independent of age. The similarities between the present findings and human studies suggest that further studies in the free-ranging rhesus macaques would provide a bridge between studies of laboratory-housed primates and studies of human beings with respect to the etiology of obesity and life-history changes in body composition and endocrine and metabolic parameters.
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PMID:Age- and gender-related changes in body size, adiposity, and endocrine and metabolic parameters in free-ranging rhesus macaques. 153 57

Obesity may be characterized by abnormal sex steroid secretion and reduced sex hormone binding globulin (SHBG) which in turn is related to fat distribution and insulin secretion. Recent in-vitro and in-vivo evidence suggests that insulin is the common mechanism regulating the secretion of SHBG and insulin-like growth factor small binding protein (IGFBP-1). IGFBP-1 appears not only to be a carrier for insulin growth factors (IGFs) but also to play an active role in growth processes, independent of growth hormone secretion. We have examined the possible relationship between fasting insulin, SHBG, testosterone, IGF-1, IGFBP-1 and fat distribution in 25 extremely obese, menstruating women (mean weight 107 +/- 3 kg) with normal glucose tolerance. Fat distribution was assessed from measurements of the waist to hip ratio (W/H). The obese women showed an elevated fasting insulin (mean +/- SEM; 21 +/- 2 mumol/l), a normal IGF-1, but reduced IGFBP-1 (14.6 +/- 2 micrograms/l); in 15 women IGFBP-1 levels were undetectable by the present assay. In addition, SHBG levels were reduced in the obese women (24 +/- 2 nmol/l) but total testosterone values (1.9 +/- 0.1 nmol/l) were normal. The elevated fasting insulin levels were positively correlated with increasing upper segment obesity as expressed by a rising W/H ratio (P less than 0.01, r2 = 0.306) and inversely correlated with SHBG (P less than 0.01, r2 = 0.483). Similarly, reduced SHBG values showed an inverse correlation with increasing W/H ratio (P less than 0.001, r2 = 0.383). No correlation was found between IGFBP-1 and W/H ratio but a strong positive correlation was seen between IGFBP-1 and SHBG (P less than 0.001, r2 = 0.466). Furthermore, an equally significant inverse correlation was found between IGFBP-1 and insulin levels (P less than 0.001, r2 = 0.474).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased sex hormone binding globulin (SHBG) and insulin-like growth factor binding protein (IGFBP-1) in extreme obesity. 170 70

IGF-1 concentrations were measured in plasma from 20 obese patients and 20 age- and sex-matched control subjects all of whom were fasting. Plasma IGF-1 concentrations were lower (p less than 0.05) in the obese individuals than in the controls. Plasma GH and insulin responses to stimulation with oral glucose were measured in 7 healthy normal weight individuals and both before and after energy restriction in 7 obese individuals. Before treatment the obese individuals were hyperinsulinaemic (fasting and integrated stimulated concentrations p less than 0.05) and showed attenuation of the plasma GH response to stimulation (peak and integrated stimulated values p less than 0.05 and less than 0.005, respectively) following oral glucose when compared to normal weight controls. Plasma insulin levels fell (both fasting and integrated concentrations p less than 0.05 and less than 0.005, respectively) and stimulated plasma GH responses increased (both peak and integrated values p less than 0.01 and less than 0.05, respectively) in the obese individuals following 3 wk treatment with a synthetic very low energy diet. Plasma IGF-1 concentrations remained unchanged during energy restriction. These results fail to support an endocrine IGF-1 mediated feedback inhibition on the hypothalamic-pituitary axis as the cause of the attenuated release of GH in obesity.
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PMID:The effect of synthetic very low calorie diets on the GH-IGF-1 axis in obese subjects. 218 1

Integrated 12-hour growth hormone secretion studies, peak growth hormone response to clonidine provocation. Somatomedin-C levels, T-4 and TSH levels were studied in six growth-retarded children with the Prader-Willi syndrome, of whom five had a 15 q-karyotype. Only one of the subjects was obese. All showed abnormally low growth hormone secretion. None achieved a nocturnal peak above 10 micrograms/l, none had a mean nocturnal level over 1.8, and none showed a level above 8 micrograms/l after clonidine provocation. These findings contrasted with normal TSH in all and normal T-4 in five. These findings suggest that the poor linear growth in the Prader-Willi syndrome is caused by a true deficiency of growth hormone secretion, and that the low growth hormone levels observed in such cases are not an artifact of obesity.
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PMID:Growth hormone secretion in Prader-Willi syndrome. 178 3

Nine patients (4F, 5M) aged 12-17 years with "fear of obesity" were studied with a sequential stimulation test utilizing insulin, LRH, TRH, and L-dopa. The comparative groups were nine female with classic anorexia nervosa, five males with undifferentiated nutritional dwarfing, and nine children (1F, 8M) with constitutional growth delay. The serum TSH, glucose, cortisol, somatotropin, prolactin, LH, and FSH were sampled periodically over 2 hours. Basal T3, T4, transferrin, and Somatomedin-C levels were also obtained. The "fear of obesity" patients did not have any pituitary function changes that were unique. These patients, as well as the comparison groups, revealed a delayed TSH response in proportion to the weight deficit which, when expressed as an integrated response, correlated well to the weight deficit for height (P less than 0.001) and to the ability to recover from hypoglycemia (p less than 0.001). The Somatomedin-C level was low and correlated to the T3 level (p less than 0.05) and not correlated to the elevated Somatotropin levels. The pituitary response to combined stimulation in patients with fear of obesity was determined to be a component of the spectrum starting at normal and proceeding to the extreme undernutrition of anorexia nervosa. Pituitary responsiveness, therefore, changes not as a function of the etiology of the malnutrition, but simply as a function of its severity.
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PMID:Pituitary-hypothalamic response in adolescents with growth failure due to fear of obesity. 310 48

We have reviewed the role of insulin in ovarian physiology. Clinical observations and experimental data strongly support the hypothesis that insulin possesses gonadotropic activity, when acting alone or with FSH or LH. This idea is further supported by the recent discovery of insulin in follicular fluid. The idea that insulin has gonadotropic function can explain a variety of clinical observations, which otherwise are difficult to understand. For example, manifestations of ovarian hypofunction (primary amenorrhea, late menarche, anovulation, low pregnancy rate, and early menopause) in IDDM can be understood if it is accepted that insulin is necessary for the ovary to reach its full steroidogenic potential. The idea that insulin affects ovarian steroidogenesis also helps to understand the observation that hyperandrogenism frequently accompanies each of the various insulin-resistant states, regardless of the latter's etiology (e.g. genetic deficiency in the number of insulin receptors, antiinsulin receptor antibodies, obesity, etc.). The explanation for this association is based on the idea that hyperinsulinemia intensifies ovarian steroidogenesis, which manifests clinically as hyperandrogenism. Continuous stimulation of the ovary by insulin over a long period of time possibly produces morphological ovarian changes, such as hyperthecosis or polycystic changes; these changes commonly are observed among women with insulin resistance. The effects of insulin on ovarian cells are mediated possibly through binding of the peptide to its own receptor or to the IGF-1 receptor (the specificity spillover phenomenon). The latter could be an important mechanism in cases of insulin resistance. Potential mechanisms underlying the gonadotropic activity of insulin include direct effects on steroidogenic enzymes, modulation of FSH or LH receptor number, synergism with FSH or LH, or nonspecific enhancement of cell viability. The gonadotropic function of insulin adds yet another note to what has been termed a symphony of insulin action. Further investigation into this new area may yield greater insights not only into normal ovarian physiology, but also into the pathogeneses of such diverse entities as PCO, obesity, diabetes mellitus, and the syndromes of insulin resistance and acanthosis nigricans.
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PMID:The gonadotropic function of insulin. 330 17

The potential was examined for insulin, growth hormone and insulin-like growth factor (IGF-1) alone or in combinations to stimulate glycerophosphate dehydrogenase (GPDH) activity, a sensitive marker of differentiation of adipose precursor cells in primary culture. Insulin, but not growth hormone or IGF-1, stimulated GPDH in the presence of fetal calf serum and cat serum. The content of growth hormone in adult rat heparinised plasma seemed, however, important for such stimulation, but was also dependent on feeding status of the plasma donor, and was abolished by hypophysectomy of the cell donor. GPDH activity was then analysed in heparinised plasma in the over-night fasting state in humans to examine a potential influence of age, obesity and pregnancy. In comparison with non-obese adults, GPDH-stimulatory activity was higher in plasma from infants and small children. A similar trend was seen in plasma from teenagers. This activity was probably partly dependent on growth hormone, because this increase of activity could be inhibited by excess of anti-human growth hormone antiserum. Obesity in adulthood or among teenagers was not associated with any difference in plasma activity to stimulate cellular differentiation, and plasma from women during late pregnancy had a low stimulating capacity. Simultaneous analyses of the potential of plasma to stimulate lipid accumulation in adipose precursor cells was proportional to the triglyceride concentration. Overall, the inhibitory effect of antihuman growth hormone antiserum on the differentiating capacity of human plasma was small or non-existing. It is therefore suggested that in human plasma, factors other than growth hormone might be important for the differentiation of adipocyte precursor cells.
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PMID:Effects of age, obesity and growth-hormone on adipogenic activity in human plasma. 331 49

Obese patients have markedly increased plasma insulin concentrations indicating insulin resistance. In contrast, plasma IGF-1 concentrations are little affected. Since the biological effects of IGF-1, including several insulin-like actions, appear to be modulated by serum carrier proteins, alterations of IGF-1 binding proteins were investigated in the serum of lean healthy individuals, and of obese patients with normal glucose tolerance. Obese patients had increased fasting plasma insulin and decreased plasma h-GH concentrations, compared to lean controls. IGF-1 concentrations were similar in both groups. Serum IGF-1 binding proteins were separated by polyacrylamide gel electrophoresis under non-reducing conditions, electroblotted onto a nitrocellulose sheet, and quantified by ligand blot with 125I IGF-1 and autoradiography. IGF-1 binding proteins of apparent molecular weight 42 kDa, 39 kDa, 35 kDa, 30 kDa and 24 kDa were observed. Obese patients had a level of IGF-1 binding proteins of 35 kDa which was decreased to 40 +/- 25% (s.d.) of control values. This 35 kDa protein corresponds to IGF-BP2, which may be involved in glucose homeostasis. It is concluded that alterations of IGF-1 binding proteins are present in obesity and may have consequences for glucose metabolism.
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PMID:Plasma IGF-1 binding proteins in lean and obese non-diabetic subjects. 768 40

The multidisciplinary, four-phase approach, which includes PSMF, BEM, and MPE is successful in treating mild, moderate, and severe degrees of childhood and adolescent obesity. The MPE program is appropriate for use with PSMF and BEM due to its progressive nature, variety of options, and moderate intensity level. In addition, the MPE program is of sufficient intensity, duration, and frequency to promote a significant increase in estimated aerobic capacity (VO2max) and to promote the maintenance of lean body mass and resting energy expenditure. The short-term intervention of PSMF, BEM, and MPE also results in an improvement in body composition, lipid profiles, and IGF-1 and T3 levels. The 1200-calorie balanced diet, MPE, and BEM also provide a successful method of weight maintenance in children and adolescents, as indicated by further improvement in body composition at the 26-week measure. Additional studies are needed to assess the contribution of exercise to the maintenance of lean body mass and resting energy expenditure in obese children and adolescents. In addition, it will be important to assess long-term weight maintenance in obese adolescents who effectively lose weight in this multidisciplinary program.
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PMID:Recent advances in the treatment of childhood obesity. 826 9

The long-term goals of our research are to understand the biochemical morbidity surrounding obstructive sleep apnea syndrome to define better the need for treatment and to determine modifiable risk factors for the disease. Our current hypothesis is that sleep-related hypoxemia results in alterations in metabolic regulatory peptides, specifically insulin and insulin-like growth factors (IGF-1 and IGF-2), which are known or suspected factors for obesity and disorders such as hypertension, glucose intolerance, and atherosclerosis. Surveys of clinic populations suggest a relationship between body habitus, parameters of sleep-disordered breathing, indices of oxygenation, and insulin resistance, defined by fasting serum levels of glucose and insulin. Results will provide insight into the role of metabolic regulatory peptides in the pathogenesis of sleep-disordered breathing and the mechanisms for this association.
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PMID:Biochemical morbidity in sleep apnea. 844 24


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