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Query: UMLS:C0948265 (metabolic syndrome)
24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years there is increasing evidence of an interaction between metabolic syndrome and testicular function. Metabolic syndrome, in particular obesity, affects testicular function by reducing total testosterone and sex hormone-binding globulin levels, as well as having a detrimental effect on spermatogenesis. On the other hand, hypogonadism further increases insulin resistance, which is the main pathophysiological feature of metabolic syndrome. There are implications that testosterone replacement can improve not only testicular function, but also parameters of the metabolic syndrome. Although the exact pathophysiological mechanisms remain unclear, leptin, resistin and ghrelin appear to play crucial roles in the interaction between metabolic syndrome and testicular function. All of this evidence supports the notion that the metabolic syndrome is a complex clinical entity characterized by pathophysiological mechanisms that affect the endocrine system as a whole; for these reasons it has been proposed to rename it 'metabolic-neuroendocrine syndrome'.
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PMID:Metabolic syndrome and reproduction: I. testicular function. 1822 42

In 1987 when Reaven introduced syndrome X (metabolic syndrome, or MS), we were studying skeletal muscle insulin resistance and found that when rodents were fed a high-fat, refined-sugar (HFS) diet, insulin resistance developed along with aspects of MS, including hyperinsulinemia, hypertension, hypertriglyceridemia, and obesity. MS was controlled in rodents by switching them to a low-fat, starch diet and was controlled in humans with a low-fat starch diet and daily exercise (Pritikin Program). Others reported inverse relations between serum insulin and sex hormone-binding globulin (SHBG). When subjects were placed on the Pritikin Program, insulin fell and SHBG rose and it was suggested that prostate cancer might also be an aspect of MS. A bioassay was developed with tumor cell lines grown in culture and stimulated with serum before and after a diet and exercise intervention. Diet and exercise altered serum factors that slowed the growth rate and induced apoptosis in androgen-dependent prostate cancer cells. Changes in serum with diet and exercise that might be important include reductions in insulin, estradiol, insulin-like growth factor-I (IGF-I), and free testosterone with increases in SHBG and IGF binding protein-1. Hyperinsulinemia stimulates liver production of IGF-I, plays a role in the promotion of prostate cancer, and thus is the cornerstone for both MS and prostate cancer. Adopting a low-fat starch diet with daily exercise controls MS and should reduce the risk of prostate cancer.
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PMID:Prostate cancer prevention by nutritional means to alleviate metabolic syndrome. 1826 84

Administration of testosterone undecanoate (TU) over 12 months to men with sexual dysfunction and signs of the metabolic syndrome, restored their plasma testosterone (T) levels to the mid-range of reference values. This had a beneficial effect on their sexual functioning as evidenced by an improvement of their scores on the International Index of Erectile Function. The scores on the Aging Male Symptoms score, AMS, were also improved. Most impressive were the improvements in the parameters of the metabolic syndrome; they all improved and appeared largely correlated (i.e., decline in waist circumference with declines of plasma cholesterol and LDL and increase in plasma HDL). Sex hormone binding globulin, SHBG, may be considered as an indicator of the severity of the metabolic syndrome; levels of SHBG initially fell, probably as a result of rising plasma T levels. But over the last six months of the observation period when plasma T rose further, there was a significant increase in plasma SHBG which may be interpreted to indicate an improvement of the metabolic syndrome. Blood pressure improved slightly but significantly. In this cohort of elderly men (54-76 years; median 64 years) there were no safety concerns over a one year period of T administration. Prostate specific antigen, PSA, levels remained stable; the International Prostate Symptoms Score, IPSS, improved slightly. Liver functions and plasma glucose remained stable. Hemoglogin and hematocrit values increased significantly but remained within reference values.
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PMID:An exploratory study of the effects of 12 month administration of the novel long-acting testosterone undecanoate on measures of sexual function and the metabolic syndrome. 1835 66

Sex steroid hormones are known to be important regulators of the lipid and glucose metabolism. Lower levels of testosterone (T) or sex hormone-binding globulin (SHBG) have been reported in men with type 2 diabetes. On the other hand, the relationship between relative hypogonadism and metabolic syndrome has not yet to be thoroughly studied. Ninety-eight Japanese adult (age 20-64) male patients with impaired glucose tolerance (IGT) or type 2 diabetes mellitus were divided into either an metabolic syndrome group (n = 42) or a non- metabolic syndrome (n = 56) group according to the definition of metabolic syndrome from WHO, or into three tertiles according to their sex hormone index level. The metabolic syndrome group had a significantly lower T/estradiol (E(2)) and SHBG level (p < 0.01). The age and subcutaneous fat surface area (SFA) were significantly different within the tertiles in SHBG and T/E(2). Logistic regression analyses were performed to investigate the association between the sex steroid hormone index level and the incidence of metabolic syndrome. Regarding the highest tertiles as a criterion, lower SHBG, T/E(2) or free T/E(2) had a higher odds ratio of prevalence of metabolic syndrome even after adjusting for age and SFA. Relative hypogonadism was strongly associated with the prevalence of metabolic syndrome in Japanese adult men who were newly diagnosed to have IGT or type 2 diabetes.
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PMID:Association between Relative Hypogonadism and Metabolic Syndrome in Newly Diagnosed Adult Male Patients with Impaired Glucose Tolerance or Type 2 Diabetes Mellitus. 1837 Jun 75

Insulin resistance, obesity, and a sex hormone alteration have each been suggested as the underlying link for the constellation of risk factors for myocardial infarction (MI) commonly referred to as the metabolic syndrome or the insulin resistance syndrome. In an attempt to identify in women which of these variables is the most likely link, insulin, adiposity variables, sex hormones, and risk factors for MI were measured and their relationships analyzed statistically in 58 premenopausal and 20 postmenopausal healthy women. On controlling for age, visceral adipose tissue (VAT) correlated more strongly with risk factors for MI, insulin, and free testosterone (FT) than did total adipose tissue or subcutaneous adipose tissue. VAT, therefore, was used as the adiposity variable for further data analysis. Waist circumference was a better surrogate of VAT than was waist-hip ratio, which was a poor surrogate of VAT. VAT correlated positively with insulin, FT, triglyceride, and glucose, and negatively with high-density lipoprotein and sex hormone-binding globulin. On controlling for age, FT and insulin correlated with risk factors for MI and with each other, but on controlling for age and VAT, all of their correlations lost statistical significance except for FT-triglyceride and FT-insulin in the postmenopausal women. In conclusion, VAT accumulation in women, independently of other measures of adiposity, may largely explain the correlations of insulin, obesity, and sex hormones with risk factors for MI and may be the immediate underlying factor that links risk factors for MI to form the metabolic syndrome. Insulin resistance, which has been generally accepted to be the underlying factor, may be a component of the syndrome rather than its underlying link. We hypothesize that in women FT may effect preferential VAT accumulation and induce insulin resistance directly, as well as via VAT accumulation, so that a sex hormone alteration may underlie VAT accumulation and thus ultimately underlie the metabolic syndrome (with insulin resistance as a component).
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PMID:Does insulin resistance, visceral adiposity, or a sex hormone alteration underlie the metabolic syndrome? Studies in women. 1850 68

Obesity is an important risk factor for many common diseases including cardiovascular disease (CVD), type 2 diabetes, cancer and erectile dysfunction (ED). Adipose tissues produce a number of adipokines and cytokines, which affect endothelial and metabolic function resulting in insulin resistance and the metabolic syndrome (risks factors for CVD). Both ED and metabolic syndrome improve with a reduction in body mass index (BMI). The relationships among obesity, metabolic syndrome, ED, sex hormone-binding globulin (SHBG) and serum total and free testosterone levels are complex and often confusing to the physician. It is known that BMI is inversely proportional to serum total testosterone concentrations; low serum SHBG levels in obesity contribute to the low serum total testosterone. Recent studies show that BMI is also inversely proportional to free testosterone concentration. The characteristic low serum testosterone concentrations observed in obese men are also present in men with the metabolic syndrome and type 2 diabetes mellitus. A small proportion of men with ED have hypogonadism; however, the proportion increases if these men are obese with manifestations of the metabolic syndrome or type 2 diabetes mellitus. ED is a common symptom in patients with type 2 diabetes who also have low testosterone levels. This review describes the relationships between low serum testosterone concentrations and ED in obese patients and those with metabolic syndrome and type 2 diabetes mellitus.
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PMID:Obesity, low testosterone levels and erectile dysfunction. 1884 73

Hypogonadism in males is a clinical syndrome complex which comprises symptoms with or without signs as well as biochemical evidence of testosterone deficiency. The diagnosis of hypogonadism thus includes both clinical history and examination as well as biochemical assessment of serum testosterone levels. Hypogonadal symptoms depend on the age at onset of hypogonadism, severity of the deficiency, its duration and sensitivity to androgen action. Prepubertal onset results in lack of virilization and pubertal development and produces features such as eunuchoid body proportions and undeveloped secondary sex characteristics. Development of hypogonadism in adult life is characterized by a loss of androgen-dependent functions such as reduction in muscle mass, a shift in body composition towards more adipose tissue, decreased sexual function with diminished libido, depressed mood, loss of psychological energy osteoporosis and several other possible symptoms. The majority of men who suffer from hypogonadism do not have classical endocrine disorders. These men present with concomitant disease such as metabolic syndrome or type 2 diabetes, chronic infections, inflammatory disease, COPD, or cardiovascular disease. All these conditions are associated with a high prevalence of hypogonadism. Pharmacological therapy with opiates and corticosteroids are also known to cause hypogonadism. Hypogonadal symptoms are precipitated at different testosterone levels. Total testosterone levels of less than 8 nmol/l highly support a diagnosis of hypogonadism whereas levels greater than 12 nmol/l are likely to be normal. The grey zone between 8 and 12 nmol/l requires further evaluation and assessment of free or non-sex hormone-binding globulin-bound (bioavailable) testosterone. A trial period of testosterone treatment may be required.
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PMID:Current guidelines for the diagnosis of testosterone deficiency. 1901 Dec 85

The increasing prevalence of metabolic syndrome (MS) with age in older men has been linked with decreasing testosterone levels. Interestingly, while testosterone levels decline with age, estradiol (E2) levels remain relatively stable, resulting in a decreased testosterone:E2 ratio. Because E2 levels tend to be elevated in morbid obesity, insulin resistance, and diabetes, it is reasonable to hypothesize that high E2 levels are associated with MS in older men. We studied the relationship of total and free E2 with MS after adjustment for multiple confounders, including age, BMI, smoking, alcohol consumption, physical activity, interleukin-6 (IL-6), fasting insulin, and testosterone. Men 65 years or older (age range, 65-96; n = 452) had complete data on E2, testosterone, fasting insulin, sex hormone-binding globulin, IL-6, and albumin. Concentrations of free E2 and free testosterone were calculated using the mass action equations. MS was defined according to Adult Treatment Panel III (ATP-III). Participants with MS had significantly higher serum free and total E2 (P < .001) (P = .003). After adjusting for confounders, including age, smoking, alcohol consumption, physical activity, log(IL-6), and log(insulin), participants with higher log(total E2) (odds ratio [OR], 2.31; 95% confidence interval [95% CI], 1.39-4.70; P = .02) and higher log(free E2) (OR, 2.69; 1.38-5.24; P < .001) had an increased risk of having MS. Log(free E2) (P = .04) maintained significant correlation with MS, even after further adjustment for BMI. In older men, high E2 is independently associated with MS. Whether confirmed in other studies, assessment of E2 should be also considered in older men. Whether changes in this hormonal pattern play a role in the development of MS should be further tested in longitudinal studies.
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PMID:Estradiol and metabolic syndrome in older italian men: The InCHIANTI Study. 1905 4

We determined serum adiponectin's role as a biomarker of metabolic syndrome (MetS), type 2 diabetes (DM) and hypertension among Turkish adults who have a high prevalence of MetS. Individuals with measured serum adiponectin concentrations, constituting a random sample of Turkish adults, were studied cross-sectionally. MetS was identified by criteria of the Adult Treatment Panel-III modified for male abdominal obesity. Median age of 547 men and 652 women was 54 years. MetS was identified in 46%. Linear regression analysis among nine variables revealed homeostatic model assessment (HOMA) index in both sexes and C-reactive protein (CRP) only in men as inversely associated covariates of adiponectin, and sex hormone-binding globulin (SHBG) as positive covariate in women. Age-adjusted sex-specifically dichotomized high vs. low adiponectin levels were significantly associated with DM (odds ratio (OR) 0.55, P = 0.01) and hypertension (OR 0.64, P = 0.012) in women, but not in men. Further adjustment for smoking status and presence of high/low BMI did not alter this sex-based relationship. As regards association with MetS, low adiponectin and high BMI interacted significantly in each sex. Yet adiponectin was associated only in men additively to the simultaneously adjusted five MetS components. We conclude that adiponectin concentrations, clearly linked to metabolic disorders, may diverge among sexes regarding protection against cardiometabolic risk through anti-inflammatory or antioxidative function, Turkish men alone revealing significant dysfunction independent of obesity. This dysfunction may underlie also the association of adiponectin levels with MetS in men to be independent of the MetS components.
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PMID:Serum adiponectin confers little protection against diabetes and hypertension in Turkish men. 1923 42

The study assessed anthropometric and laboratory variables, in particular testosterone (T) in a group of obese men of <40 years. Of 60 men with a body mass index (BMI) of >27 kg m(-2), 34 met the criteria of the metabolic syndrome (MS). Twenty men <40 years (with a BMI <25 kg m(-2)) were studied for comparison. It was found that with increasing BMI, levels of serum leptin, triglycerides, insulin, the ratio high-density lipoprotein (HDL) cholesterol/low-density liporotein (LDL) cholesterol, the waist circumference (WC), the area of visceral fat and systolic/diastolic blood pressure were higher, whereas insulin sensitivity (HOMA) and serum T were lower. Obesity (BMI 27-30 kg m(-2)) was associated with a decline in plasma T, but not with a decline in plasma sex hormone-binding globulin (SHBG). The latter was the case in more severe obesity (>30 kg m(-2)) qualifying as MS. In patients with MS, 58% variability of T levels could be predicted by combination of independent factors - SHBG, ratio LDL/HDL, insulin and leptin. On the other hand, in men with MS, 80% variance of concentrations of SHBG were predicted by triglycerides, HDL, glucose, leptin and surface of visceral adipose tissue. It is concluded that plasma T is significantly correlated with a number of features of the MS and, therefore, plasma T could serve as a marker of the MS.
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PMID:Testosterone and obesity in men under the age of 40 years. 1926 Aug 42

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