Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal. Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3. untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension). States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome. The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.
 ...
PMID:Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. 1205 88

Obesity is associated with different disturbances in endocrine function. Both spontaneous growth hormone (GH) secretion and its response to several stimuli have shown to be reduced in obese patients. The GH responses to GH-releasing hormone and other challenges by pyridostigmine suggest that the reduction in GH secretion is related to an increased somatostatinergic tone. Other experiments point to a down-regulation of somatostatin receptors in the somatotroph cell. Ghrelin administration is followed by a massive GH release, but the possibility that ghrelin or GHRH deficiency are the cause of GH deficiency in obesity is unlikely. The increase in free fatty acids in obesity might be related to GH reduction, since acipimox administration is able to reverse GH secretion. In women, abdominal obesity is associated with hyperandrogenism and low sex hormone-binding globulin levels. Obese men have low testosterone and gonadotrophin concentrations, specially in cases of morbid obesity. An increase in hypothalamic-pituitary-adrenal axis activity and some resistance to dexamethasone suppression have been described in abdominal obesity. This effect may be due to neuroendocrine alterations related to a genetic origin. Adrenal hyperfunction may favour cardiovascular and metabolic complications. There are no disturbances in thyroid function. Sometimes a reduction in prolactin response to several stimuli has been reported. This effect may be due to hyperinsulinaemia or to disturbances in the dopaminergic tone.
 ...
PMID:[Neuroendocrine disturbances in obesity]. 1538 10