Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid hormone picture of 28 patients (15 males and 13 females), mean age 56.6 yr (range 45-65 yr), with seriously decompensated type II diabetes mellitus has been studied. In each patient the study was repeated after 3 months of treatment of diabetes. The patients showed significantly lower serum T3 levels and significantly higher serum rT3 levels (P less than 0.001), in comparison with a group of 16 normoglicemic subjects. After 3 months of strict control of diabetes T3 and FT3 significantly increased (P less than 0.01), whereas significant variations of rT3 were not found. Among the whole group of diabetics 5 patients had low levels of serum T4 (P less than 0.01 vs. controls), high levels of serum TSH (P less than 0.001 vs. controls) and an exaggerated responsiveness to exogenous TRH (P less than 0.001 vs. controls). After the 3 months of treatment these patients showed a significant decrease of rT3 (P less than 0.02) and of delta-TSH (P less than 0.01). In the whole group of diabetics significant statistical correlations between glycometabolic and thyroid parameters were not found. The study, on the whole, showed in patients with seriously decompensated type II diabetes, a hormone picture like the low-T3 syndrome, in some cases, however, pituitary TSH secretion suggested the existence of incipient failure of thyroid hormones. A connection between alterations in thyroid hormone picture and glycometabolic imbalance, even statistically labile, is however indicated by improvement of thyroid function when diabetes is carefully controlled.
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PMID:[Changes in the thyroid hormone picture that may be found in severely decompensated type II diabetics]. 200 Jan 80

Pancreatic islet cell, thyroid, gastric parietal cell, and adrenal autoantibodies were studied in 110 young insulin-dependent diabetics (type I; IDDM), 12 non-insulin-dependent diabetics (NIDDM), 26 patients with pancreatic diabetes, and 123 age- and sex-matched healthy controls. All the patients were aged 30 years or under at the onset of diabetes. Islet cell antibody was found in 31% of the patients with IDDM, but in only one patient with NIDDM, one patient with pancreatic diabetes, and one healthy control subject. Thyroid, parietal cell, and/or adrenal antibodies were present in 26% of the IDDM patients, 17% of the NIDDM patients, 12% of the patients with pancreatic diabetes, and 19% of the control subjects. There was no association between the presence of islet cell antibody and other organ-specific autoantibodies and any particular HLA phenotype. Data from the North Indian study have been compared with those from other populations of the world, similarities and differences have been brought out, and their significance has been discussed. The relative contribution of the autoimmune component in the etiopathogenesis of different forms of diabetes mellitus varies among the different populations of the world, accounting to some extent for the observed differences in incidence and clinical profiles.
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PMID:Autoimmunity in type I (insulin-dependent) diabetes mellitus in North India. 703 29

The proband, a 9-year-old Hispanic female, presented with hair loss, strabismus, and weight gain. On magnetic resonance imaging (MRI) she was found to have severe primary hypothyroidism and a large pituitary mass. In addition, acanthosis nigricans, obesity, and hyperinsulinism were observed. Findings were similar in three of four siblings. Thyroid peroxidase antibodies were detected in the father and three of four siblings. Although all family members were obese, and hyperinsulinemia with high proinsulin and C-peptide was found in all except one sibling, only the mother and one child had overt type 2 diabetes mellitus. Because of the unusual association of autoimmune thyroid disease, insulin resistance and obesity rather than insulin deficiency, we searched for possible genetic abnormalities. The HLA haplotypes did not cosegregate with autoimmune thyroid disease or insulin resistance. Mutational analysis of known obesity genes was done. Leptin was not deficient, and sequencing of the proband's DNA showed no mutations in the perixisome proliferator activated receptor (PPAR)-gamma, PPAR-gamma(2), PPAR-alpha or melanocortin 4 receptor genes. Maternally inherited diabetes and deafness was ruled out since no mutations were found in mitochondria DNA. Insulin receptor antibodies were not detected. In conclusion, the remarkably high incidence of childhood autoimmune hypothyroidism, pituitary enlargement, insulin resistance and obesity in this family is not linked to known HLA types or known gene defects.
Thyroid 2004 Apr
PMID:Familial juvenile autoimmune hypothyroidism, pituitary enlargement, obesity, and insulin resistance. 1514 66

The aim of our study was to evaluate antibodies against thyroglobulin (anti-TG) and thyroid peroxidase (anti-TPO) - markers of autoimmune thyroiditis - in several groups of adult patients with type 1 and type 2 diabetes mellitus (DM). We were particularly interested whether the presence of thyroid antibodies is related to the positivity of glutamic acid decarboxylase antibodies (anti-GAD). We found elevated anti-GAD in 46 % (97/210) patients with type 1 DM. All patients with type 2 diabetes were anti-GAD-negative. At least one thyroid antibody (anti-TG and/or anti-TPO) was found in 30 % (62/210) patients with type 1 DM and 27 % (22/83) type 2 diabetes patients. The patients with type 1 DM were further grouped according to their anti-GAD status. The anti-GAD-positive patients had a higher prevalence of anti-TG antibodies than the anti-GAD-negative patients (25 % vs. 12 %, p=0.03) as well as anti-TPO antibodies (32 % vs. 12 %, p<0.001). At least one thyroid antibody was detected in 39 % (38/97) of anti-GAD-positive but only in 21 % (24/113) of anti-GAD-negative patients with type 1 DM (p=0.006). No significant difference in the frequency of thyroid antibodies was found between anti-GAD-negative patients with type 1 and type 2 DM (21 % vs. 27 %, p=0.4). The groups with or without thyroid antibodies in both type 1 and type 2 diabetic patients did not differ in actual age, the age at diabetes onset, duration of diabetes, body mass index or HbA1c level. Patients with elevated thyroid antibodies had significantly higher levels of TSH than those without thyroid antibodies (1.86 vs. 3.22 mIU/l, p=0.04 in type 1 DM; 2.06 vs. 4.89 mIU/l, p=0.003 in type 2 DM). We conclude that there is a higher frequency of thyroid-specific antibodies in anti-GAD-positive adult patients with type 1 DM than in anti-GAD-negative patients or in patients with type 2 DM. Patients with or without thyroid antibodies do not differ in age, DM onset and duration, BMI or HbA1c. Thyroid antibodies-positive patients have higher levels of thyroid stimulating hormone (TSH).
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PMID:Anti-GAD-positive patients with type 1 diabetes mellitus have higher prevalence of autoimmune thyroiditis than anti-GAD-negative patients with type 1 and type 2 diabetes mellitus. 1520 35

A common polymorphism of the type 2 deiodinase gene (Thr92Ala DIO2) was found to be associated with insulin resistance in a mixed Caucasian population. The aim of this study was to investigate the association of the Thr92Ala DIO2 variant to indices of insulin resistance in the Old Order Amish. A genotype-phenotype association study was performed at the research clinic in Strasburg, Pennsylvania, and the molecular genetics laboratory at the University of Maryland, Baltimore, Maryland, and the National Institutes of Health, Bethesda, Maryland. A total of 1,268 subjects participated in the Amish Family Diabetes Study. An association among the Thr92Ala DIO2 variant and type 2 diabetes, indices of insulin resistance (HOMA-IR), insulin secretion, free thyroid hormones, and thyrotropin (TSH) was found. No association was found among the Thr92Ala DIO2 variant and type 2 diabetes, impaired glucose tolerance, or body mass index (BMI) in the Amish. In nondiabetics (n = 747), the Ala92 allele tended to be associated with decreased rather then increased insulin secretion. No differences were observed in thyroid hormones or TSH. Contrary to prior findings, the Thr92Ala DIO2 variant tends to be associated with increased rather then decreased insulin sensitivity in the Amish. These findings could be secondary to a different genetic background or to environmental factors specific for this population.
Thyroid 2005 Nov
PMID:The Thr92Ala deiodinase type 2 (DIO2) variant is not associated with type 2 diabetes or indices of insulin resistance in the old order of Amish. 1635 84

Hyperglycemic hyperosmolar state (HHS) is an acute complication mostly occurring in elderly type 2 diabetes mellitus (DM). Thyrotoxicosis causes dramatic increase of glycogen degradation and/or gluconeogenesis and enhances breakdown of triglycerides. Thus, in general, it augments glucose intolerance in diabetic patients. A 23-yr-old female patient with Graves' disease and type 2 DM, complying with methimazole and insulin injection, had symptoms of nausea, polyuria and generalized weakness. Her serum glucose and osmolarity were 32.7 mM/L, and 321 mosm/kg, respectively. Thyroid function tests revealed that she had more aggravated hyperthyroid status; 0.01 mU/L TSH and 2.78 pM/L free T3 (reference range, 0.17-4.05, 0.31-0.62, respectively) than when she was discharged two weeks before (0.12 mU/L TSH and 1.41 pM/L free T3). Being diagnosed as HHS and refractory Graves' hyperthyroidism, she was treated successfully with intravenous fluids, insulin and high doses of methimazole (90 mg daily). Here, we described the case of a woman with Graves' disease and type 2 DM developing to HHS.
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PMID:A case of hyperglycemic hyperosmolar state associated with Graves' hyperthyroidism: a case report. 1689 29

After a long history of relative neglect by the scientific community, white adipose tissue is finally emerging as a central component of body homeostasis. Indeed, the explosion of obesity statistics worldwide encouraged the study of adipose tissue and the complications of increased adiposity, such as insulin resistance, type 2 diabetes, and accelerated vascular disease. Far beyond merely furnishing free fatty acids from triglyceride depots, a growing list of fat tissue-derived mediators has increased the understanding of the regulatory role of adipose tissue in metabolic control. Recently, inflammation within the obese adipose tissue has surfaced as another important link of obesity to its undesirable metabolic consequences.
Thyroid 2008 Feb
PMID:The multiple facets of the fat tissue. 1827 18

A key phenotype associated with type 2 diabetes in humans is impaired mitochondrial oxidative metabolism in skeletal muscle, a pattern potentially contributing to increased lipid accumulation and impaired metabolic flexibility-in turn, central features of both insulin resistance and diabetes. Since thyroid hormone regulates mitochondrial gene expression and function in skeletal muscle, reductions in T3-mediated transcription may contribute to diabetes-related impairments in oxidative metabolism. We review the evidence for relationships between thyroid hormone action and diabetes risk, and discuss potential mechanisms linking intracellular thyroid hormone availability, thyroid receptor action, and the transcriptional coactivator PGC1 in regulating oxidative metabolism.
Thyroid 2008 Feb
PMID:Links between thyroid hormone action, oxidative metabolism, and diabetes risk? 1827 23

Thyroid dysfunction was assessed in an older population-based cohort with type 2 diabetes. Among type 2 diabetes subjects, 7.1% had incident thyroid dysfunction versus 3.8% in those without diabetes (odds ratio 1.97, 95% confidence interval 0.88-4.38). Screening of thyroid dysfunction in older diabetes subjects is not supported by these findings.
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PMID:Type 2 diabetes does not predict incident thyroid dysfunction in the elderly. 1883 87

Thyroid associated ophthalmopathy (TAO), a cardinal clinical pointer to diagnose Graves' disease (GD), is seen less frequently in our country than in the West, but can have sight threatening consequences. Smoking, diabetes, male gender, increasing age and radioactive iodine treatment for thyrotoxicosis are known precipitating factors for TAO. We report four cases of thiazolidinediones (TZD) precipitated TAO. All were male, had autoimmune thyroid disease (three had Graves' disease and one had Hashimoto's thyroiditis) and type 2 diabetes mellitus (T2DM). They developed eye symptoms three to four months after taking TZDs for glycaemic control. Two of them responded to medical treatment, the other two underwent surgical decompression.
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PMID:Thiazolidinedione precipitated thyroid associated ophthalmopathy. 2104 86


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