Dependence of Hypothalamic Obesity on Insulin, the Pituitary and the Adrenal Gland.
Summary:The obesity which follows destruction of the ventromedial nucleus (VMN) of the hypothalamus of rats is accompanied by hyperphagia and hypersecretion of insulin. The identical response of streptozotocin-treated control and VMN lesioned rats to insulin suggests that the obesity which follows hypothalamic damage results directly from a hypersecretion of insulin which in turn induces a secondary hyperphagia. (Endocrinology 90: 885, 1972)
http://endo.endojournals.org/cgi/content/abstract/90/4/885
Hypothalamic obesity. The autonomic hypothesis and the lateral hypothalamus.
Several lines of evidence support the hypothesis that derangements in the function of the autonomic nervous system play an important role in the development of hypothalamic obesity. Vagotomy below the diaphragm, reverses the syndrome. In diabetic rats cured of their diabetes with transplants of fetal pancreatic tissue beneath the renal capsule, ventromedial hypothalamic (VMH) lesions do not produce the characteristic rise in food intake nor do they significantly increase serum insulin. These observations indicate that the hyperinsulinaemia following VMH lesions is the result of neural connections rather than from a circulating humoral factor released following VMH injury.
http://www.ncbi.nlm.nih.gov/pubmed/7014333
Autonomic Unbalance and the Metabolic Syndrome: Hypothesis: The Unbalanced Autonomic Nervous System Causes the Symptoms of the Metabolic Syndrome.
The metabolic syndrome consists of visceral obesity, hyperglycemia, hyperinsulinemia, dyslipidemia, and cardiovascular diseases. A common pathophysiological denominator underlying these epidemiological correlations has not been identified. However, the autonomic nervous system was shown to play a role in the metabolic syndrome
http://www.medscape.com/viewarticle/464264_5
Leptin and Androgens in Male Obesity: Evidence for Leptin Contribution to Reduced Androgen Levels.
Leptin circulates in plasma at concentrations that parallel the amount of fat reserves. In obese males, androgen levels decline in proportion to the degree of obesity. In conclusion, our studies, together with previous in vitro findings, indicate that excess of circulating leptin may be an important contributor to the development of reduced androgens in male obesity.
http://jcem.endojournals.org/cgi/content/abstract/84/10/3673
Chorionic Gonadotropin in Obesity Further Clinical Observations.
After 40 years of trying every new approach to the treatment of obesity with little or no success, I believe a new method that works has been made available to us. It works with about 60-70% of obese patients of both sexes aged 15 and up, provided the method is followed meticulously as the author has developed it. No one can yet say for certain how or why it works, and a great deal of research will be needed. I hope that this report of my own clinical findings together with some possible tentative explanations will act as a stimulus for this research.
http://www.ajcn.org/cgi/content/abstract/22/6/686
Bioavailability of hCG after intramuscular or subcutaneous injection in obese and non-obese women.
Examination of the hCG plasma concentration–time curve showed the area under the curve (AUC) and maximum concentration (Cmax) of hCG to be significantly higher after i.m. injection than after s.c. injection in both the obese and non-obese groups. However, the AUC and Cmax values in obese women were significantly lower than in non-obese women, irrespective of whether i.m. or s.c. dosing was employed. Intramuscular dosing of hCG provided better bioavailability than s.c. dosing, but bioavailability was significantly less in obese women than in non-obese women.
http://humrep.oxfordjournals.org/cgi/content/abstract/18/11/2294
Up-Regulation of Placental Leptin by Human Chorionic Gonadotropin.
Leptin, the 16,000 molecular weight protein product of the obese gene, was originally considered as an adipocyte-derived signaling molecule for the central control of metabolism. In conclusion, weprovide some evidence suggesting that hCG induces leptin expression in trophoblastic cells probably involving the MAPK signal transduction pathway
http://endo.endojournals.org/cgi/reprint/150/1/304
In vitro effects of chorionic gonadotropin hormone on human adipose development.
It is well known that pregnancy is associated with fat weight gain. However, the mechanisms whereby fat mass accumulation is controlled during this period are poorly understood. Therefore, we attempted to determine whether human chorionic gonadotropin (HCG), in vitro, influences human adipose tissue development and/or metabolism. Finally, HCG significantly stimulates the secretion of the proadipogenic factor, leptin, from human adipose tissue. Taken altogether, these data suggest that the proadipogenic effect of HCG in human preadipocytes contributes to explain why increased fat storage occurs during the first trimester of pregnancy.
http://joe.endocrinology-journals.org/cgi/content/abstract/194/2/313
