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

Insulin resistance is a cause for morning hyperglycemia seen in diabetic patients. Other reasons for morning hyperglycemia should be eliminated by performing an insulin response test. Once insulin resistance has been established as the cause of hyperglycemia, a step-by-step process should be used to establish the cause of the insulin resistance. Common causes of insulin resistance include hyperadrenocorticism, acromegaly, hyperthyroidism, and obesity. Hepatic disease, renal insufficiency, and sepsis are other causes of insulin resistance in practice. Less common causes include insulin antibodies, pregnancy, neoplasia, hyperandrogenism, and pheochromocytoma. If the underlying cause cannot be found or resolved, then increased doses of insulin are required to manage the hyperglycemia.
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PMID:Problems in diabetes mellitus management. Insulin resistance. 213 77

Androgens are a family of steroids hormones secreted by the adrenal glands and the ovaries in women. The adrenal secretion of androgens becomes significant around the age of 7, at the onset of adrenal activity, and increases until ovarian puberty. The excess of adrenal androgens, of which the main products are dehydroepiandrosterone and its ester sulfate (DHEAS), is unrelated to a classic deficiency of steroid biosynthesis. Blocking with small doses of dexamethasone (0.5 then 0.25 mg at night), demonstrates that the DHEAS may be blocked and rules out a tumor of the adrenal cortex. This treatment, which presents tolerance problems, is effective on acne, but ineffective on hirsutism which requires the use of antiandrogens. In addition to this idiopathic adrenal hyperandrogenism, the late manifestations of a congenital deficiency in 21-hydroxylase in a clinical picture varying from a mere obesity to moderate hirsutism, but may evolve to a syndrome of polycystic ovaries, is easy to diagnose with a basic 17-hydroxyprogesterone assay. In this case, adrenal blocking by dexamethasone often gives a spectacular clinical result. Isolated ovarian hyperandrogenism, is found in the various clinical forms of the polycystic ovaries syndrome. Usually, this syndrome is suggested by the anovulation, cause of sterility, hirsutism and overweight. Ovarian ultrasonography is often difficult to explain, particularly because of the non-univocal macroscopic appearance of the ovaries. Therefore, a great deal of emphasis is placed on the hormonal exploration which shows an elevated concentration of serum testosterone (T) and mostly of delta-4 androstenedione (A), combined with an elevated luteinizing hormone (LH) which should be determined on several successive samples.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyperandrogenism in premenopausal women]. 218 98

Resistance to insulin consists in a decrease in insulin's biologic action and is manifested mainly by hyperinsulinism. Clinical investigation of insulin resistance states relies on specialized tests, performed both in vitro and in vivo. The hyperinsulinemic-euglycemic clamp is the reference method for quantifying insulin resistance and can differentiate decreased insulin sensitivity and decreased maximal capacity for glucose uptake. Glucose flux measurements, using glucose labelled with stable isotopes, distinguish hepatic and peripheral factors involved in insulin resistance. In vitro studies include investigations for antibodies against insulin and insulin receptors, studies of insulin receptors and their tyrosine kinase activity, and studies of postreceptor cell metabolism. These investigations are especially useful in genetic syndromes of extreme insulin resistance, whose pathophysiology is largely unelucidated, including: insulin resistance syndromes with acanthosis nigricans, obesity-acanthosis nigricans-hyperandrogenism syndrome, lipoatrophic diabetes, leprechaunism, and other syndromes. But insulin resistance also plays a major role in non-insulin-dependent diabetes mellitus, insulin-dependent diabetes mellitus, and various pathological or even physiological endocrine alterations.
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PMID:[Hyperinsulinism syndromes caused by insulin resistance]. 219 May 20

Hirsutism as a sign of hyperandrogenism is a common endocrinological disorder in women. Its spectrum varies from mild forms with dominating psychic component to severe forms associated with virilization. The severity should be assessed by semiobjective scoring systems, the use of which also allows the systematic follow-up of the results of treatment. An increase in serum androgen levels or an increased turnover of androgens can be detected in most patients. Enhanced peripheral conversion of androgens to locally acting androgen also leads to hirsutism. The thorough investigation of the endocrinological milieu is required to rule out androgen producing neoplasms. In most patient, however, disturbances are functional, among which polycystic ovary syndrome is the commonest. It is a disorder exhibiting a complexity of changes in endocrinological interactions. Besides inappropriate gonadotropin secretion insulin and insulin like growth factor are also involved. The opioidergic system also seems to be affected. Polycystic ovary syndrome is also associated with obesity and infertility, both of which require attention.
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PMID:Hirsutism: definitions and etiology. 219 64

Androgens arise from either adrenal or ovarian secretion or by peripheral conversion of secreted precursors. The adrenals and ovaries normally contribute about equally to testosterone and AD production. DHAS is the major adrenal 17-KS. Testosterone is the major circulating form of androgen. More than 96% of plasma testosterone is bound to SHBG; the free testosterone seems to be the bioavailable fraction. Hyperandrogenism must be considered in any girl with premature or excessive development of public hair or acne, menstrual irregularity (whether it be oligo-amenorrhea or dysfunctional uterine bleeding), or obesity. The most common cause of premature public hair development (pubarche) is premature adrenarche. The most common cause of hyperandrogenism presenting in a teenage girl is polycystic ovary syndrome. However, the differential diagnosis includes "exaggerated adrenarche," late-onset congenital adrenal hyperplasia, virilizing tumors, Cushing's syndrome, hyperprolactinemia, acromegaly, and abnormalities of androgen action or of metabolism. The plasma free testosterone is a more sensitive indicator of hyperandrogenism than is the total testosterone concentration. The pattern of response of plasma free testosterone, DHAS, and cortisol to dex-suppression testing is diagnostic of the source of androgen excess. Most hyperandrogenic adolescents will be found to have PCOS. The treatment is chosen according to particular symptoms, such as menstrual irregularity, hirsutism, or obesity.
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PMID:Hyperandrogenism in peripubertal girls. 225 43

Polycystic ovary syndrome is a disorder of unknown cause characterized by anovulation, hyperandrogenism, and gonadotropin secretory abnormalities producing oligo-ovulation or anovulation. Hyperinsulinemia and insulin resistance are important features of this syndrome. Because other causes of androgen excess may produce similar clinical and biochemical findings, PCO remains a diagnosis of exclusion. Treatment is directed toward relieving symptoms of hyperandrogenemia in order to stimulate ovulation, correcting obesity, and inducing regular menses to reduce the risk of endometrial cancer.
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PMID:Polycystic ovary syndrome. 226 12

We studied a group of obese hyperandrogenic amenorrheic women to determine the effects of weight loss on anthropometry, hormonal status, menstrual cycles, ovulation, and fertility. Fourteen women had polycystic ovaries, two the hyperandrogenism-insulin resistance-acanthosis nigricans syndrome, one hirsutism of adrenal origin, and three idiopathic chronic anovulation. The duration of amenorrhea before the study ranged from 3-17 months [mean, 8.6 +/- 4.5 (+/- SD)]. All women ate a hypocaloric diet for a period of 8.0 +/- 2.4 months. Weight loss ranged from 4.8 to 15.2 kg (mean, 9.7 +/- 3.1 kg; 1.35 +/- 0.56 kg/month) and the waist to hip ratio, which was used as a measurement of body fat distribution, decreased from 0.86 +/- 0.1 to 0.81 +/- 0.06 (P less than 0.0001). The women's mean plasma testosterone and LH concentrations decreased significantly (P less than 0.001 and P less than 0.005, respectively). A significant positive correlation was found between the decreases in plasma testosterone levels and the decreases in glucose-stimulated insulin levels. Moreover, the decreases in the waist to hip ratio correlated positively with the decreases in glucose-stimulated insulin levels and inversely with the decreases in plasma 17 beta-estradiol. No relationships were found between weight loss and the changes in plasma insulin, steroid, and gonadotropin concentrations. The responsiveness to the weight reduction program was evaluated by comparing the number of menstrual cycles during the study period with the number reported before it. Eight women had significantly improved menstrual cyclicity (responders), while 12 did not (nonresponders). The clinical characteristics and hormone values were similar in responder and nonresponder women. In the group as a whole, 33% of the menstrual cycles during the study were ovulatory, and 4 pregnancies occurred. Hirsutism improved significantly in more than half of the women, as did acanthosis nigricans when present. We conclude that weight loss is beneficial in all obese hyperandrogenic women regardless of the presence of polycystic ovaries, the degree of hyperandrogenism, and the degree and distribution of obesity.
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PMID:Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss. 264 85

It is important to diagnose hyperandrogenism in women. By disturbing ovulation, it is actually one of the most frequent causes of infertility. In this particular case, its diagnosis has specific implications: sometimes specific treatment is indicated, or the risk of fetal virilization should be prevented. There is always the possibility of a diagnosis of polycystic ovary, prompting precautionary measures to be taken that are likely to limit the risks linked to the multifollicular development that is so frequent with this disorder. In addition, hyperandrogenism exposes the patient to various gynecological and general complications: cancer of the endometrium, progressive increase in menstrual disturbances and infertility, obesity, metabolic disturbances and probably increase in cardiovascular risks. Certain types of hyperandrogenism give rise to diseases that expose the patient to specific risks: virilizing tumors, Cushing's syndrome, neonatal risks linked to congenital hyperplasia of the adrenal glands. Hyperandrogenism should be borne in mind not only when the clinical picture is that of virilization, but also when there is any disturbance in eugonadal ovulation, whether or not this is manifested as menstrual disturbances or as infertility, and especially whether or not it is accompanied by hirsutism.
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PMID:[When and why should hyperandrogenism be searched for in women?]. 267 67

Insulin resistance and hyperinsulinemia appear to be almost universal features of the polycystic ovary syndrome. We propose that obesity permits full phenotypic expression of the polycystic ovary syndrome in women predisposed to develop this condition by generating an insulin-resistant, and consequently hyperinsulinemic, state. The resultant hyperinsulinemia may produce hyperandrogenism by affecting multiple facets of androgen metabolism.
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PMID:The central role of obesity (hyperinsulinemia) in the pathogenesis of the polycystic ovary syndrome. 268 38

The relationship between sex hormones and the skin is increasingly considered to be very important. The skin has appropriately been called "A peripheral endocrine gland". In this review some aspects of the cutaneous metabolism of oestrogens, progestogens and particularly androgens are analyzed. Production of skin collagen is markedly enhanced by oestrogens. Progestogens with strong androgenic activity and especially androgens have a powerful stimulating action on all skin elements particularly the epidermis and the dermis the sebaceous glands and the hair. The skin manifestations of hyperandrogenism and disturbances of reproductive functions such as anovulation, oligoamenorrhoea and polycystic ovarian disease are usually the consequences of three main aetiopathogenic factors: the first is an abnormality of GnRH pulsatility related to central nervous system dysfunction and seemingly mediated by an increase in beta Endorphin, possibly related to some extent to changes in body weight and hyperinsulinism. The second aetiopathogenic approach is hyperaestronaemia secondary to obesity. Finally adrenal hyperandrogenism caused by different types of congenital adrenal hyperplasia or by increased sensitivity to ACTH may be implicated in these various clinical manifestations.
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PMID:[Sex hormones and the skin]. 269 19


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