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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Upper body obesity and the related metabolic disorder type 2 diabetes have been identified as risk factors for breast cancer, and associated with late-stage disease and a poor prognosis. Components of the metabolic syndrome, including visceral adiposity, insulin resistance, hyperglycemia and hyperinsulinemia, with or without clinically manifest diabetes mellitus, low serum high-density lipoprotein cholesterol and hypertension have all been related to increased breast cancer risk. The biochemical mechanisms include extraglandular oestrogen production, reduced sex hormone-binding globulin with consequent elevation of the bioactive plasma free oestradiol and increased insulin biosynthesis, all of which exert mitogenic effects on both untransformed and neoplastic breast epithelial cells. Obesity, type 2 diabetes and the metabolic syndrome also have in common an increased production of leptin and a decreased production of adiponectin by adipose tissue, with consequent elevations and reductions, respectively, in the circulating levels of these two adipokines. These changes in plasma leptin and adiponectin, acting through endocrine and paracrine mechanisms, have been associated in several studies with an increase in breast cancer risk and, perhaps, to more aggressive tumours; studies in vitro showed that leptin stimulates, and adiponectin inhibits, tumour cell proliferation and the microvessel angiogenesis which is essential for breast cancer development and progression.
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PMID:Adiposity, type 2 diabetes and the metabolic syndrome in breast cancer. 1771 97

This study investigated the role of relative androgen excess, designated by low sex hormone-binding globulin (SHBG), on development of type 2 diabetes in premenopausal African American women. A prospective, longitudinal study was conducted on premenopausal African American women, initially aged 36 to 43 years (n=119). Patients were reexamined 8 years later to determine whether initial androgen status was associated with insulin resistance and development of diabetes. Among patients in the low SHBG tertile, 18% converted to type 2 diabetes by the second examination, as compared with 5% in the mid SHBG tertile and 2.5% in the high SHBG tertile (P=.04). Insulin sensitivity was significantly different among the 3 tertiles (P<.01). There was no significant difference in total cholesterol, high-density lipoprotein, low-density lipoprotein, or triglycerides among the SHBG tertiles. This prospective study demonstrates that relative androgen excess is associated with insulin resistance and increases the risk for development of diabetes in premenopausal African American women.
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PMID:Androgen excess is associated with insulin resistance and the development of diabetes in African American women. 1805 8

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

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

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

Over the last three decades it has become apparent that testosterone plays a significant role in the maintenance of bone and muscle mass, in erythropoiesis, and in mental functions. But testosterone is also a key player in glucose homeostasis and lipid metabolism. The metabolic syndrome is a clustering of risk factors predisposing to late onset diabetes mellitus, atherosclerosis and cardiovascular morbidity and mortality. The main components of the syndrome are visceral obesity, glucose intolerance, raised blood pressure and dyslipidaemia (elevated triglycerides, low levels of high-density lipoprotein cholesterol),and a pro-inflammatory and thrombogenic state. Cross-sectional epidemiological studies have reported a direct correlation between plasma testosterone and insulin sensitivity, and low testosterone levels are associated with an increased risk of type 2 diabetes mellitus, dramatically illustrated by androgen deprivation in men with prostate carcinoma. Lower total testosterone and sex hormone-binding globulin(SHBG) predict a higher incidence of the metabolic syndrome. There is now evidence to argue that hypotestosteronaemia should be an element in the definition of the metabolic syndrome. Administration of testosterone to hypogonadal men reverses the unfavorable risk profile for the development of diabetes and atherosclerosis. Testosterone should be regarded as a pivotal hormone for men's health.
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PMID:The role of testosterone in the metabolic syndrome: a review. 1944 34

Obesity in men, particularly when central, is associated with lower total testosterone [TT], free testosterone [FT] and sex hormone-binding globulin [SHBG], and a greater decline in TT and FT with increasing age compared with lean men. Obesity-related conditions such as obstructive sleep apnea, insulin resistance and type 2 diabetes mellitus are independently associated with decreased plasma testosterone. Possible mechanisms include decreased LH pulse amplitude, inhibitory effects of oestrogen at the hypothalamus and pituitary and the effects of leptin and other peptides centrally and on Leydig cells. Obese men have reduced sperm concentration and total sperm count compared to lean men but sperm motility and morphology appear unaffected. The cause and effect relationships between low plasma androgen levels, obesity and the metabolic syndrome, and associated cardiometabolic risk remain unclear. While weight loss normalizes TT and FT in obese men, androgen replacement in the short term does not significantly improve cardiometabolic risk profile despite reducing fat mass.
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PMID:Obesity and testicular function. 1954 Mar 7

Retinol-binding protein 4 (RBP4) is a newly discovered adipokine, which is reported to be correlated with insulin resistance (IR) and type 2 diabetes (T2DM). The aim of this study was to evaluate the influence of menopausal status on RBP4 concentration and to investigate serum RBP4 with IR and the prevalence of T2DM in postmenopausal women. We conducted a cross-sectional study and enrolled 34 healthy premenopausal women, 41 healthy postmenopausal women and 37 postmenopausal women with T2DM. Serum RBP4 concentration was measured by an enzyme-linked immunosorbent assay. Anthropometric parameters, plasma glucose, insulin and sex hormones concentrations were measured, and IR was assessed by HOMA2-IR. We found RBP4 was significantly elevated after menopause, even after adjustment for age and BMI. In postmenopausal women, RBP4 correlated positively with BMI, WHR, FPI, HOMA2-IR, TG and FAI, while negatively with SHBG (p<0.05). Furthermore, RBP4 was positively associated with 17beta-estradiol in only diabetic postmenopausal women. In healthy premenopausal group, age, BMI, and TG were the independent determinants of RBP4. In two postmenopausal groups, the independent determinants of RBP4 were BMI, WHR, HOMA2-IR, TG and FAI in healthy subjects, and in group with T2DM, the determinants were BMI, WHR, FPI, HOMA2-IR, TG and FAI (p<0.05). However, serum RBP4 was not significantly associated with increased odds of T2DM in postmenopausal women (OR 0.979, 95% CI 0.610-1.637). The findings suggested serum RBP4 concentration is influenced by menopausal status and closely related to IR but not to the prevalence of T2DM in postmenopausal women.
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PMID:Serum retinol-binding protein 4 is elevated and positively associated with insulin resistance in postmenopausal women. 1967 94

OBJECTIVE Insulin resistance is greater in racial/ethnic minorities than in non-Hispanic whites (NHWs) for those with and without type 2 diabetes. Because previous research on insulin resistance in type 1 diabetes was limited to NHWs, racial/ethnic variation in an estimated measure of insulin resistance in type 1 diabetes was determined. RESEARCH DESIGN AND METHODS The sample included 79 individuals with type 1 diabetes diagnosed at age <18 years (32.9% NHWs, 46.8% non-Hispanic black [NHB], 7.6% other/mixed, and 12.7% Hispanic) and their families. Estimated glucose disposal rate (eGDR) (milligrams per kilogram per minute; a lower eGDR indicates greater insulin resistance) was calculated using A1C, waist circumference, and hypertension status. RESULTS Mean current age was 13.5 years (range 3.2-32.5) and diabetes duration was 5.7 years (0.1-19.9). eGDR was inversely associated with age. Compared with that in NHWs, age-adjusted eGDR was significantly lower among nonwhites (NHB, other/mixed, and Hispanic: Delta = -1.83, P = 0.0006). Age-adjusted eGDR was negatively associated with body fat, triglycerides, urinary albumin/creatinine, acanthosis nigricans, parental obesity, and parental insulin resistance and positively related to HDL and sex hormone-binding globulin. In multivariable analysis, lower eGDR was significantly associated with older age, nonwhite race/ethnicity, acanthosis, and lower HDL. CONCLUSIONS Minorities with type 1 diabetes are significantly more insulin resistant, as measured by eGDR, than NHWs. Exploring potential mechanisms, including disparities in care and/or physiological variation, may contribute to preventing racial/ethnic differences in insulin resistance-associated outcomes.
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PMID:Racial and ethnic differences in an estimated measure of insulin resistance among individuals with type 1 diabetes. 2000 42


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