Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A fictitious patient with obesity, hirsutism and polycystic ovary syndrome is discussed by 3 British general practitioners to illuminate management of this type of case. The patient is 24 years old, expects to marry next year, has irregular menses averaging 6 weeks apart, and is requesting an explanation for her irregular periods as well as oral contraception. The 1st physician would exclude hypothyroidism, then evaluate polycystic ovary syndrome by assaying testosterone, LH, FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the grounds that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an essay of sex hormone binding globulin and the LH:FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the ground that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an assay of sex hormone binding globulin and the LH:FSH ration between Days 2-6 of the cycle, and rule out congenital adrenal hyperplasia with an assay for 17-alpha-OH-progesterone. Since the patient might be anovulatory because of obesity, major long-term weight lose is a priority. Prescription of pills would depend on family history, smoking, and the degree of hirsutism and endocrine status. The most likely prescription would be a reverse sequential of cyproterone acetate 50 or 100 mcg from Days 5-15, and ethinyl estradiol 30 mcg on Days 2-25.
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PMID:Contraception and irregular menses. 259 23

The aim of our work was to investigate a possible role of protein kinase C (PKC) in insulin-stimulated glucose uptake in mouse skeletal muscle, and to search for a defect in PKC activation in insulin resistance found in obesity. In isolated soleus muscle of lean mice, insulin (100 nM) and 12-O-tetradecanoylphorbol 13-acetate (TPA) (1 microM) acutely stimulated glucose uptake 3- and 2-fold respectively. The effects of insulin and TPA were not additive. When PKC activity was down-regulated by long-term (24 h) TPA pretreatment, before measurement of glucose transport, the TPA effect was abolished, but in addition insulin-stimulated glucose transport returned to basal values. Furthermore, polymyxin B, which inhibits PKC in muscle extracts, prevented insulin-stimulated glucose uptake in muscle. In muscle of obese insulin-resistant mice, glucose uptake evoked by insulin was decreased, whereas the TPA effect, expressed as a fold increase, was unaltered. Thus both agents stimulated glucose transport to the same extent. Furthermore, no difference was observed when PKC activation by TPA was measured in muscle from lean and obese mice. These results suggest that: (1) PKC is involved in the insulin effect on glucose transport in muscle; (2) PKC activation explains only part of the insulin stimulation of glucose transport; (3) the defect in insulin response in obese mice does not appear to be due to an alteration in the PKC-dependent component of glucose transport. We propose that insulin stimulation of glucose uptake occurs by a sequential two-step mechanism, with first translocation of transporters to the plasma membrane, which is PKC dependent, and second, activation of the glucose transporters. In obesity only the activation step was decreased, whereas the translocation step was unaltered.
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PMID:Insulin-stimulated glucose transport in muscle. Evidence for a protein-kinase-C-dependent component which is unaltered in insulin-resistant mice. 264 84

In general, rises in systolic blood pressure to over 200 mm Hg during exercise with a workload of 100W are regarded as pathological. Excessive exercise blood pressure values are to be expected in principle in all hypertensives. However, there are so far no generally accepted criteria for diagnosis of isolated systolic exercise hypertension (with normal values of resting blood pressure). The incidence of isolated systolic exercise hypertension is estimated to be about 10% of a selected population. In patients with excessive rises in blood pressure during exercise who want to engage actively in sport, general measures (reduction of obesity, restriction of alcohol and salt intake) and endurance training should be recommended initially. For endurance training, sporting activities that involve dynamic exercise are to be recommended (walking, running, mountain hiking, cycling, swimming, cross-country skiing). Activities involving isometric exercise (rowing, diving, tennis) and sport of a competitive nature are not suitable. In moderately severe and severe hypertension (diastolic blood pressure values in excess of 105 mm Hg), sporting activities and endurance training are contraindicated. If the exercise blood pressure values cannot be lowered below 220 mm Hg with the general measures mentioned, pharmacotherapy is to be considered. The drugs of choice for suppressing excessive rises in blood pressure during exercise are beta-blockers. In this group, beta 1-blockers are to be preferred to non-selective beta-blockers because of the metabolic neutrality of the former. beta-Blockers without intrinsic sympathomimetic activity (ISA) lower the blood pressure-pulse rate product more effectively than beta-blockers with ISA. Alternatively, calcium antagonists of the verapamil type and ACE inhibitors can be employed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of hypertension in actively exercising patients. Implications for drug selection. 264 57

Dysfunctional uterine bleeding is classified by the character of the menstrual cycle: ovulatory or anovulatory. Anovulation can occur at any age and is physiologic in the first year or two after menarche and for several years before menopause. Anovulatory cycles are characteristically irregular and marked by prolonged episodes of bleeding unassociated with signs or symptoms of ovulation. Specific causes of anovulation such as hyperprolactinemia, thyroid disease, androgen excess, anorexia, obesity, and excess exercise can be treated specifically; otherwise, therapy depends upon patient goals. Cycle regulation can be affected by monthly courses of progestin, such as medroxyprogesterone acetate (Provera), 10 mg daily for 10 days each month. Contraception and cycle regulation can both be accomplished with oral contraceptives. Fertility, on the other hand, will require ovulation induction. Ovulatory dysfunctional uterine bleeding most prevalent in parous women between the ages of 20 and 40 is associated with regular cycle intervals and premenstrual molimina. Midcycle and perimenstrual spotting can often be treated with observation only, but depending upon patient and/or physician concerns, periodic hormonal suppression is effective. The management of menorrhagia should include the following: (1) exclusion of pathology in the genital tract; (2) reduction in activity during days of heavy flow; (3) the avoidance of aspirin in the week before and on days of flow; (4) nonsteroidal anti-inflammatory drugs; (5) cycle suppression--oral contraceptives, danazol (Danocrine), depo-progestin; (6) luteal phase progestin; and (7) surgical intervention.
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PMID:Dysfunctional uterine bleeding. 305 63

Adrenalectomy arrests the development of obesity in ob/ob mice fed nonpurified high-starch diets partly by stimulating the low thermogenic activity of brown adipose tissue (BAT). However, adrenalectomy fails to suppress the development of obesity in ob/ob mice fed a purified high-glucose diet. Effects of adrenalectomy on BAT metabolism in ob/ob mice fed purified high-starch or high-glucose diets were therefore examined. Adrenalectomy markedly decreased the efficiency of energy retention and increased BAT metabolism (as assessed by GDP binding to BAT mitochondria, GDP-inhibitable acetate- or chloride-induced mitochondrial swelling, and by rates of norepinephrine turnover in BAT) in ob/ob mice fed a high-starch purified diet but had only minimal effects on energy efficiency or BAT metabolism in ob/ob mice fed a high-glucose purified diet. Plasma insulin concentrations decreased and thyroxine concentrations increased in adrenalectomized ob/ob mice fed the high-starch diet; changes in these hormones were less pronounced in adrenalectomized ob/ob mice fed the high-glucose diet. Consumption of glucose mimics effects of adrenal secretions on BAT metabolism in ob/ob mice.
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PMID:Adrenalectomy fails to stimulate brown adipose tissue metabolism in ob/ob mice fed glucose. 318 36

It was found that in the livers of db/db mice with hyperinsulinemia, obesity and non-insulin-dependent diabetes the rates of cholesterol biosynthesis from pyruvate and, to a lesser extent, from acetate and mevalonate as well as of cholesterol ester biosynthesis from pyruvate (but not from acetate and mevalonate) are increased. Presumably, the observed changes are mediated by structural alterations in the CoA reserves, i.e., increase of free CoA to short-chain acyl-CoA and free CoA to long-chain fatty acyl-CoA indices, and of the ratio between enzymatic activities of generation and utilization of NADPH. Treatment of db/db mice with phosphopantothenate, besides eliciting changes in the CoA reserves structure towards normalization and inhibition of NADP-dependent dehydrogenases and pyruvate and 2-oxoglutarate dehydrogenase complexes, causes the diminution of cholesterol and its ester levels in the liver in the absence of any conspicuous changes in the rates of their biosynthesis from pyruvate.
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PMID:[Effect of phosphopantothenate on the biosynthesis of cholesterol and its esters from various precursors in the liver of db/db mice]. 325 47

Adult female rats were fed, in addition to chow and water, a carbohydrate source that differed in type (glucose, sucrose, or polysaccharide), form (32% solution, powder, or gel), or taste (very sweet, minimally sweet, or bitter). A control group was fed only chow and water during the 40-day experiment. The groups fed the glucose solution, sucrose solution, or one of three polysaccharide solutions (Polycose, maltose-dextrin 10, maltose-dextrin 42) all overrate and gained more body weight and fat than did the control group. The carbohydrate solution groups did not differ in their total caloric intake, weight gain, percent body fat, or basal insulin level. The polysaccharide groups, however, consumed more carbohydrate than did the sugar groups. The groups fed glucose, sucrose, or Polycose in powder form consumed less carbohydrate and total calories, gained less weight and fat, and had lower insulin levels than did the groups fed the saccharides in solution form. The powder groups did not reliably differ from the control group on these measures. Rats fed Polycose in solution form or in a solid gel form (32% Polycose + 1% agar) were similar in their carbohydrate intake, total caloric intake, weight gain, and percent body fat. Rats fed Polycose solutions that were minimally sweet (32% Polycose), sweet (0.2% saccharin + 32% Polycose), or bitter [0.05% sucrose octa acetate (SOA) + 32% Polycose] did not differ in their Polycose intake, total caloric intake, weight gain, or percent body fat. The results demonstrate that saccharide form is more important than saccharide type or taste in promoting hyperphagia and obesity in rats. The Polycose gel findings further indicate that it is the water of hydration, not liquidity that is responsible for the hyperphagia-inducing effect of carbohydrate solutions.
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PMID:Carbohydrate-induced hyperphagia and obesity in the rat: effects of saccharide type, form, and taste. 330 91

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

Synthetic progestins derived from nortestosterone provide a promising contraceptive alternative for women with contraindications for estrogens. Progesterone and synthetic progestins reduce vasodilatation and edema induced by estrogens and stop estrogen-dependent cellular multiplication in target tissue. Progestins have 2 kinds of contraceptive affect: antigonadotropic action at sufficient doses, and peripheral action at lower doses. The cervical mucus is modified in composition and volume, becoming hostile to sperm; the endometrial mucus atrophies; and tubal motility is slowed. High dose progestins are administered from the 5th or 10th to the 25th cycle day, with the earlier date preferred for women with shorter cycles. They are an ideal method for women with endometrial hyperplasia or benign breast disease or histories of breast or uterine cancer, as well as for women over 40 with dysovulatory cycles. Contraindications to high dose progestins include obesity, hypertension, lipid metabolic anomalies, and diabetes. Low dose progestin-only pills are administered at the exact same time each day including during menstruation. They are attractive for some women because they contain no estrogen, a reduced progestin dose causing fewer headaches and less somnolence, and fewer metabolic effects. Low dose progestins are indicated for lactating women, those with contraindications to estrogens such as obesity, hypertension, hyperlipidemia, and diabetes, and those with renal or cardiac insufficiency with valvulopathy. Low dose progestins are also indicated for nulliparas and other women for whom IUDS are contraindicated. Women using low dose progestins should never take drugs that act as enzymatic inductors, which speed hepatic degradation of steroids and reduce their efficiency. A resulting pregnancy is likely to be extrauterine because of slowed tubal transport. The failure rate of low dose progestins ranges from .9-3%, with higher failure rates among younger women. About 30% of users initially experience spotting, which despite its usual disappearance after 2-3 months of use is the most common reason for discontinuing the method. Low dose progestins have no metabolic or vascular effects, but they may cause a relative hyperestrogenism is some users. Other modes of administration of progestin contraception include continuous high doses, never justified solely for contraception. Trimonthly injections of medroxyprogesterone acetate of norethindrone enanthate provide contraception through a long lasting antigonadotropic effect. Metrorrhagia and amenorrhea are among possible side effects. The method is used primarily in developing countries where its ease of use is a major advantage. Subcutaneous implants releasing continuous doses of levonorgestrel provide contraceptive protection for over 5 years. The cumulative failure rate is 1.7 at 5 years. Metabolic tolerance is good. The major side effect is menstrual irregularity.
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PMID:[Progestational contraception]. 365 94

Diet-induced obesity in rats can be produced by high-fat feeding. Comparing high-fat with low-fat feeding, the present study was designed to characterize the phases of development of obesity. In the dynamic phase, male rats were investigated at the age of 9-10 weeks after feeding the diets for 4-5 weeks. In the static phase, the animals at the age of 24-26 weeks were tested after 20-22 weeks of the nutritional regime. In this phase, the effects of switching high-fat to low-fat diet for 4 weeks were also examined. Fractionating lipid extracts by thin layer chromatography the concentrations of several lipids in epididymal adipose tissue, in serum, and in liver were determined. In liver, the enhancement of cholesteryl-ester (CE) concentration after high-fat feeding besides the accumulation of triglycerides (TG) is remarkable. Cell fractionation studies of the livers by differential ultracentrifugation showed the major part of the accumulated CE in the supernatant. In vitro incorporation of (1-14C)acetate and (2-14C)mevalonate into liver slices indicated that cholesterol synthesis in the liver of the obese rats was not increased. Although the offered fat diet with 0.1% of cholesterol can not be considered as high in cholesterol, the 2.5-fold higher amount of the high-fat diet in comparison with the low-fat diet (0.04% cholesterol) could be responsible for the enlargement of CE in the liver of the fat fed rats. This possibility was proved by measurement of the cholesterol absorption and transport to the liver after oral administration of (4-14C)cholesterol. Estimation of TG secretion rates of the liver using Triton WR 1339 pointed out higher rates in the obese rats in the dynamic phase. In the static phase, the rates were not different between both feeding groups, while fat restriction in the food produced a striking increase of TG secretion. It is assumed that only in the dynamic phase metabolism is able to compensate the liver TG accumulation by an enhanced transport to the adipose tissue. In the static phase this ability is diminished but not lost.
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PMID:Some aspects of lipid metabolism in the liver of Wistar rats with fat diet-induced obesity. 403 42


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