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

Diabetes may be associated with many genetic disorders. The scientific importance of these often rare disorders resides in the insight they may provide into the possible mechanisms of common diabetes. The type of diabetes varies in these syndromes. Non-insulin-dependent diabetes (NIDDM), clinically similar to common NIDDM, may be found in some syndromes (e.g. Werner's syndrome). In others there may be considerable insulin resistance, such as that present in ataxia telangiectasia. Extreme insulin resistance due to abnormal insulin receptor function is found in the Mendenhall syndrome. The mechanism of diabetes is more obscure in acute intermittent porphyria (AIP), although haem deficiency affecting the cytochrome chain raises interesting possibilities. In glycogen storage disease type I, the diabetes is associated with insulinopenia, following an earlier period in the disease when hypoglycaemia is the rule. IDDM, clinically similar to the common form, is present in the autoimmune polyglandular syndromes. Although a change in the lean:fat ratio is common in many neuromuscular disorders, mechanisms other than insulin resistance would seem to operate. The increased incidence of diabetes in heterozygotes for some of these genetic disorders raises the possibility that many common diabetics are, in fact, heterozygotes for some other disorder. The increased frequency of diabetes in Klinefelter's syndrome, Turner's syndrome and possibly Down's syndrome leads to the hypothesis that non-disjunction may, in some way be associated with the predisposition to diabetes. In several syndromes there is an increased incidence of diabetes in otherwise unaffected relatives of individuals with these syndromes. It is impossible to assess what proportion of common NIDDM or IDDM is made up of heterozygotes for these genetic syndromes.
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PMID:Diabetes secondary to genetic disorders. 144 74

A 37 year-old female with Kallmann syndrome and NIDDM who had two successful deliveries is reported. She had experienced no menstruation until she had treatment with gestagen in her early twenties. She had withdrawal bleeding only once. At the age of 25, she consulted her family doctor, complaining of amenorrhea. Estrogen progesterone cyclic therapy caused withdrawal bleeding, and clomiphene citrate failed to induce apparent ovulation. In January 1978, 150 IU of hMG was administered daily for 9 days, and then 3000 IU of hCG daily for the following 2 days. This therapy induced pregnancy, which failed spontaneously on June 4th. A year later, in January 1979, 150 IU of hMG was again administered daily for 7 days followed by 6000 IU of hCG for 3 days. This therapy again induced pregnancy. On September 27th, 1979, she delivered a girl vaginally, weighing 3830 g. After this delivery, she experienced no menstruation. In June 1985, she consulted her family doctor again, and she was diagnosed as being pregnant. Since her fasting blood glucose was 145 mg/dl, she was admitted to Kosei Hospital to control her blood glucose. On October 15th, she delivered a girl weighing 2600 g. On June 13th, 1989, she was referred to Kosei Hospital by her family doctor to achieve an accurate control of her blood glucose. During this admission, she was diagnosed as having Kallmann syndrome because of congenital anosmia and hypogonadotropic hypogonadism without any abnormal morphological changes. Vitamin B1 infusion test was negative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of two successful deliveries by a woman with Kallmann syndrome and NIDDM]. 190 34

A successful GnRH treatment for hypogonadotropic hypogonadism is described. A 40 year old infertile patient due to Kallmann's syndrome, associated with obesity and NIDDM, was treated with HCG (5,000 IU/week) for 8 years. In an attempt to induce spermatogenesis HMG (75 IU/daily) was added for 2 years. During the combined gonadotropin treatment semen analysis indicated an improvement from azoospermia to 2 x 10(6) sperm/ml. Since semen quality remained poor and obviously no pregnancy was achieved, the last regime was replaced by a pulsatile GnRH treatment (5 mcg/90 minutes). Following 6 months sperm count increased up to 15 x 10(6) associated with normal motility and morphology. Patient's wife conceived after the second intrauterine insemination and delivered a full term healthy baby.
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PMID:Successful GnRH treatment in a patient with Kallmann's syndrome, who previously failed HMG/HCG treatment. 314 74

A 46-year-old Japanese male was admitted for the evaluation of severe hypertension. He was obese and had a eunuchoidal body habitus. Chromosomal analysis revealed a 46, XY/47, XXY karyotype. Serum LH, FSH and testosterone levels were low, indicating hypogonadotropic hypogonadism. Endocrinological dynamic tests disclosed presence of hypothalamic panhypopituitarism, partial diabetes insipidus, type 2 diabetes mellitus and low renin essential hypertension. Brain computed tomography and magnetic resonance imaging revealed intra- and extrasellar masses. Histological examination of the tissue obtained at transsphenoidal surgery showed a Rathke's cleft cyst (RCC). To the best of our knowledge, this is the first case report of mosaic Klinefelter's syndrome accompanied by symptomatic RCC, type 2 diabetes mellitus and low renin essential hypertension.
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PMID:Multiple endocrine disorders and Rathke's cleft cyst with Klinefelter's syndrome: a case report. 1240 86

Type 2 diabetes is associated with lower total testosterone (T) levels in cross-sectional studies. However, it is not known whether the defect is primary or secondary. We investigated the prevalence of hypogonadism in type 2 diabetes by measuring serum total T, free T (FT), SHBG, LH, FSH, and prolactin (PRL) in 103 type 2 diabetes patients. FT was measured by equilibrium dialysis. FT was also calculated by using T and SHBG (cFT). Hypogonadism was defined as low FT or cFT. The mean age was 54.7 +/- 1.1 yr, mean body mass index (BMI) was 33.4 +/- 0.8 kg/m(2), and mean HbA1c was 8.4 +/- 0.2%. The mean T was 12.19 +/- 0.50 nmol/liter (351.7 +/- 14.4 ng/dl), SHBG was 27.89 +/- 1.65 nmol/liter, and FT was 0.250 +/- 0.014 nmol/liter. Thirty-three percent of patients were hypogonadal. LH and FSH levels were significantly lower in the hypogonadal group compared with patients with normal FT levels (3.15 +/- 0.26 vs. 3.91 +/- 0.24 mIU/ml for LH and 4.25 +/- 0.45 vs. 5.53 +/- 0.40 mIU/ml for FSH; P < 0.05). There was a significant inverse correlation of BMI with FT (r = -0.382; P < 0.01) and T (r = -0.327; P < 0.01). SHBG correlated inversely with BMI (r = -0.267; P < 0.05) but positively with age (r = 0.538; P < 0.001) and T (r = 0.574; P < 0.001). FT correlated strongly with cFT (r = 0.919; P < 0.001) but not with SHBG. LH levels correlated positively with FT (r = 0.287; P < 0.05). We conclude that hypogonadotropic hypogonadism occurs commonly in type 2 diabetes.
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PMID:Frequent occurrence of hypogonadotropic hypogonadism in type 2 diabetes. 1575 66

Our understanding of the effect of androgens on insulin action and glucose metabolism is incomplete. Several different models and methods have been used to study androgen effects, with some studies indicating that higher testosterone levels are associated with increased insulin resistance. In polycystic ovary syndrome, where high testosterone levels are frequently found, affected patients have a higher risk of diabetes. In contrast, increased insulin resistance was found in both hypergonadotropic and hypogonadotropic men with hypoandrogenism, patients with Klinefelter's syndrome and men with idiopathic gonadotropin deficiency. Insulin resistance is considered to be one of the cornerstones in the state that ultimately leads to clinically established type 2 diabetes mellitus. In addition, men with type 2 diabetes have relative hypogonadism. Therefore, supplementation with testosterone might play a role in improving both insulin resistance and hypogonadism. The study population consisted of 11 male patients with type 2 diabetes. Their mean age was 57.7 +/- 3.41 years, the body mass index (BMI) was 24.4 +/- 1.02 kg/m2, and the waist-to-hip ratio (W/H) was 0.91 +/- 0.05. The patients were all treated with oral hypoglycemic agents. The men received androgen injections every 3 weeks intramuscularly for 12 weeks. The injections were testosterone depot 100 mg/3 weeks. Insulin sensitivity, glucose effectiveness and area under acute insulin response were calculated from "minimal model" algorithms. There were no significant differences in the value of BMI, W/H ratios, plasma lipid concentrations, testosterone, homeostasis model assessment (HOMA) of insulin sensitivity, and beta-cell function, before and after supplementation of testosterone. Furthermore, the insulin sensitivity (SI) (1.04 +/- 0.25, 1.11 +/- 0.36 x 10(-5) min(-1/)pM; p = 0.43), glucose effectiveness (EG) (0.018 +/- 0.003, 0.017 +/- 0.002 min(-1); p = 0.29), and acute insulin response (AIR) after a glucose load (45.7 +/- 24.3, 50.1 +/- 32.5 pM; p = 0.45) did not change significantly after supplmentation with testosterone. In our study, there was no improvement of SI, EG, and AIR after 3 months of Testosterone Depot treatment in type 2 diabetes, but we believe that duration and dosage of the androgen therapy might play an important role in improving insulin sensitivity. The mechanisms by which testosterone causes insulin resistance is unknown, and larger studies on androgen treatment in type 2 diabetic patients are necessary.
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PMID:The effect of testosterone supplement on insulin sensitivity, glucose effectiveness, and acute insulin response after glucose load in male type 2 diabetics. 1635 72

Metabolic syndrome is characterized by insulin insensitivity, central obesity dyslipidemia, and hypertension. It is recognized as a risk factor for cardiovascular disease in men; by the time metabolic syndrome is diagnosed, however, most men already have entrenched cardiovascular disease. A reliable early warning sign is needed to alert physicians to those at risk for metabolic syndrome and cardiovascular disease. Low serum testosterone level has emerged as a reliable prognosticator of metabolic syndrome in men whose testosterone deficiency is genetic (Klinefelter syndrome), iatrogenic following surgery for testicular cancer, pharmacologically induced by gonadotropin-releasing hormone during prostate cancer treatment, or a natural consequence of aging. One third of men with type 2 diabetes mellitus are now recognized as testosterone deficient. Emerging evidence suggests that testosterone therapy may be able to reverse some aspects of metabolic syndrome.
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PMID:Testosterone, diabetes mellitus, and the metabolic syndrome. 1804 26

It has recently been demonstrated that > or = one-third of men with type 2 diabetes mellitus have low testosterone concentrations associated with inappropriately low luteinizing hormone and follicle-stimulating hormone concentrations. Hypogonadotropic hypogonadism in men with type 2 diabetes is associated with obesity but not duration of diabetes, elevated glycosylated hemoglobin, or the presence of microvascular complications of diabetes. Recent data show that hypogonadotropic hypogonadism is also observed frequently in nondiabetics with the metabolic syndrome or obesity, but it is not associated with type 1 diabetes. Low testosterone concentrations in men with type 2 diabetes have also been related to a higher C-reactive protein concentrations, lower hematocrit, increased total and regional adiposity, lower bone mineral density, and erectile dysfunction. This article discusses the pathophysiology of hypogonadotropic hypogonadism in men with type 2 diabetes and its signs and symptoms. Clinical trials are required to determine whether testosterone replacement therapy alleviates insulin resistance, inflammation, and symptoms related to sexual dysfunction care.
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PMID:Hypogonadotropic hypogonadism in men with type 2 diabetes. 1949 39

Hypogonadism occurs commonly in men with type 2 diabetes (T2DM) and severe obesity. Current evidence points to a decreased secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus and thereby decreased secretion of gonadotropins from the pituitary gland as a central feature of the pathophysiology in these men. Hyperglycaemia, inflammation, leptin and oestrogen-related feedback have been proposed to make aetiological contributions to the hypogonadotropic hypogonadism of T2DM. However, the neuroendocrine signals that link these factors with modulation of GnRH neurons have yet to be identified. Kisspeptins play a central role in the modulation of GnRH secretion and, thus, downstream regulation of gonadotropins and testosterone secretion in men. Inactivating mutations of the kisspeptin receptor have been shown to cause hypogonadotropic hypogonadism in man, whilst an activating mutation is associated with precocious puberty. Data from studies in experimental animals link kisspeptin expression with individual factors known to regulate GnRH secretion, including hyperglycaemia, inflammation, leptin and oestrogen. We therefore hypothesise that decreased endogenous kisspeptin secretion is the common central pathway that links metabolic and endocrine factors in the pathology of testosterone deficiency seen in men with obesity and T2DM. We propose that the kisspeptin system plays a central role in integrating a range of metabolic inputs, thus constituting the link between energy status with the hypothalamic-pituitary-gonadal axis, and put forward potential clinical studies to test the hypothesis.
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PMID:Hypothesis: kisspeptin mediates male hypogonadism in obesity and type 2 diabetes. 2062 62

There is a higher prevalence of low testosterone levels in males with type 2 diabetes compared to those without. Additionally, there is evidence that low testosterone levels may predict the development of type 2 diabetes. Symptoms of hypogonadism include decreased libido, decreased bone mineral density (BMD), and decreased lean muscle mass. The majority of the published cases in men with diabetes were attributed to age-related idiopathic hypogonadotropic hypogonadism. This paper reviews the link between type 2 diabetes and age-related hypogonadism and the treatment options for hypogonadism. Pharmacists who provide care for males with diabetes should be aware of the increased incidence of hypogonadism, know how to screen for it, and be able to recommend appropriate therapy.
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PMID:Age-related androgen deficiency and type 2 diabetes. 2167 55


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