Polycystic ovary syndrome and the androgen-insulin connection

Article Abstract:

The polycystic ovary syndrome, also known as the Stein-Leventhal syndrome, is an endocrine disorder characterized by the absence of ovulation (the release of the egg from the ovaries) and by the formation of many cysts in the ovaries. It is caused by the persistent stimulation of the ovary by the luteinizing hormone, which is released from the pituitary gland. The luteinizing hormone activates the development of the corpus luteum, a yellow body in the ovary formed after the ovary releases the egg. The polycystic ovary syndrome is associated with insulin resistance, the lack of tissue response to insulin; hyperandrogenism, or increased levels of androgens, hormones that activate the development of male characteristics; and hyperinsulinemia, increased blood levels of insulin. Hyperinsulinemia may lead to the development of acanthosis nigricans, an inflammatory skin disease, which is characterized by papillary growths, discoloration, and overgrowth of the horny layer of the outer skin. A possible mechanism explaining the relationship between hyperandrogenism, insulin resistance, and the polycystic ovary syndrome is described. Increased blood levels of insulin associated with insulin resistance may increase the release of androgens from the ovary. The androgens may promote the accumulation and increase the size of fat cells in the abdomen, leading to android obesity, in which there is more fat in the waist than in the hip. Studies have shown a relation between android obesity and non-insulin-dependent diabetes mellitus. In addition, androgens may impair the actions of insulin on the liver and peripheral tissues, interfere with the removal of insulin by the liver, and reduce the sensitivity of the liver and peripheral tissue to insulin. These actions of androgen may thus contribute to the persistence of insulin resistance and hyperinsulinemia. (Consumer Summary produced by Reliance Medical Information, Inc.)

Insulin resistance, Androgens

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Release of tumor necrosis factor alpha by human peritoneal macrophages in response to toxic shock syndrome toxin-1

Article Abstract:

Toxic shock syndrome is a rare and potentially lethal condition caused by toxic substances released by the bacteria Staphylococcus aureus. The disorder is characterized by high fever; a widespread red, spotty rash that later results in shedding or flaking of the skin from the soles and palms; and low blood pressure, and dizziness. In addition, toxic shock syndrome may also be associated with vomiting or diarrhea; severe muscle pain; and abnormalities of the mucous membranes, kidney, liver, blood, and central nervous system. One of the toxic substances released by S. aureus is exotoxin toxic shock syndrome toxin-1 (TSST-1), which can cause fever and effects on the immune system. Endotoxin, another toxic substance from bacteria, causes the release of tumor necrosis factor alpha (TNF-alpha) from monocytes, a type of white blood cell, and macrophages, cells associated with the immune system. TNF-alpha causes symptoms that are very similar to those of toxic shock syndrome. The effect of TSST-1 on the release of TNF-alpha from monocytes and macrophages was assessed. Monocytes and macrophages were obtained from four healthy women and from 22 women who underwent laparoscopy, the internal examination of the abdomen using a tube-like device with an optical system. TSST-1 caused the release of TNF-alpha from macrophages and monocytes. The release of TNF-alpha by macrophages was increased in women with endometriosis (the abnormal development of endometrial tissue that normally lines the uterus) at various sites in the pelvis and abdomen. These findings show that TSST-1 can cause the release of TNF-alpha from monocytes and macrophages, and indicates that TNF-alpha may be responsible for the abnormalities associated with toxic shock syndrome. (Consumer Summary produced by Reliance Medical Information, Inc.)

Bacterial toxins, Tumor necrosis factor, Toxic shock syndrome

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The relationship between circulating androgens, obesity, and hyperinsulemia on serum insulin-with growth factor binding protein-1 in the polycystic ovarian syndrome

Article Abstract:

Chronic overproduction of androgen in women with polycystic ovarian syndrome does not appear to regulate levels of circulating insulin-like growth factor binding protein-1 (IGFBP-1). Male hormones are produced in the ovary under the stimulation of insulin-like growth factor-1. Since IGFBP-1 binds this growth factor and renders it inactive, it was thought that a chronic overabundance of androgen would be associated with reduced levels of IGFBP-1. Sixteen women with polycystic ovarian syndrome participated. Nine patients were obese. All had some facial hair and menstruated rarely or not at all. All had an intravenous glucose tolerance test, and blood samples were periodically taken and analyzed for IGFBP-1, male hormones, glucose, insulin, luteinizing hormone, estrogens, and cortisol. The patient's weight and the patient's insulin response to glucose were the only factors related to lower levels of IGFBP-1.

Obesity, Insulin-like growth factor 1, Insulin-like growth factor I

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