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

Recent studies indicate that serum levels of osteocalcin, a 49-aminoacid bone matrix protein, are a biochemical marker of bone formation. In order to study bone metabolism in diabetes mellitus, in 28 patients with Type 1 (insulin-dependent) diabetes mellitus, in 38 patients with Type 2 (non-insulin-dependent) diabetes mellitus and two control groups, matched for Type 1 and Type 2 diabetic patients, respectively, serum levels of osteocalcin, parathyroid hormone and 25 hydroxy vitamin D were measured by radioimmunoassay. Whereas in Type 1 diabetic patients and control subjects serum levels of osteocalcin and 25 hydroxy vitamin D were not statistically different, serum osteocalcin and 25 hydroxy vitamin D levels were significantly decreased in Type 2 diabetic patients when compared with corresponding control subjects (p less than 0.03 and p less than 0.001, respectively). Independent of the type of diabetes, serum parathyroid hormone levels were comparable in diabetic patients and matched control subjects. Serum osteocalcin levels were significantly lower in Type 1 diabetic patients with retinopathy and/or proteinuria than in Type 1 diabetic patients without microangiopathy (p less than 0.05). Whereas serum parathyroid hormone levels in Type 2 diabetic patients with retinopathy and/or proteinuria were significantly increased (p less than 0.02), 25 hydroxy vitamin D levels were decreased (p less than 0.02) when compared with Type 2 diabetic patients without microangiopathy. Our data give evidence of a vitamin D deficiency and a decreased bone formation in patients with Type 2 diabetes mellitus. In Type 1 diabetes mellitus bone formation as reflected by serum osteocalcin levels is influenced by the presence or absence of microangiopathic complications.
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PMID:Serum osteocalcin levels in diabetes mellitus: analysis of the type of diabetes and microvascular complications. 326 86

The derangement of glucose metabolism is found frequently in all forms of hyperparathyroidism. Both in primary (PHPT) and secondary hyperparathyroidism (SHPT) PTH excess is thought to be involved in deteriorating insulin sensitivity and secretion though their different clinical and pathophysiological conditions. In PHPT these abnormalities are related to a high frequency of Type 2 diabetes mellitus and also impaired glucose tolerance according to recent clinical studies, without differences between symptomatic and asymptomatic clinical presentation. In chronic renal failure (CRF), the disorders of glucose metabolism due to SHPT do not bear an increased risk for diabetes whereas they seem to be involved in the progression of atherosclerotic vascular damage which connotes CRF. Moreover, clinical and experimental studies have shown that vitamin D deficiency associated with glucose metabolism abnormalities favors the development of the metabolic syndrome. The potential for metabolic and cardiovascular harm related to hyperparathyroidism, especially PHPT, is the most interesting issue for clinical endocrinologists. This short review of the clinical and pathophysiological data of literature on glucose homeostasis disorders in hyperparathyroidism focuses on its potential clinical and therapeutic impact, particularly in the management of PHPT.
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PMID:Derangement of glucose metabolism in hyperparathyroidism. 1500 55

This review summarizes current knowledge on vitamin D status in the elderly with special attention to definition and prevalence of vitamin D insufficiency and deficiency, relationships between vitamin D status and various diseases common in the elderly, and the effects of intervention with vitamin D or vitamin D and calcium. Individual vitamin D status is usually estimated by measuring plasma 25-hydroxyvitamin D (25OHD) levels. However, reference values from normal populations are not applicable for the definition of vitamin D insufficiency or deficiency. Instead vitamin D insufficiency is defined as the lowest threshold value for plasma 25OHD (around 50 nmol/l) that prevents secondary hyperparathyroidism, increased bone turnover, bone mineral loss, or seasonal variations in plasma PTH. Vitamin D deficiency is defined as values below 25 nmol/l. Using these definitions vitamin D deficiency is common among community-dwelling elderly in the developed countries at higher latitudes and very common among institutionalized elderly, geriatric patients and patients with hip fractures. Vitamin D deficiency is an established risk factor for osteoporosis, falls and fractures. Clinical trials have demonstrated that 800 IU (20 microg) per day of vitamin D in combination with 1200 mg calcium effectively reduces the risk of falls and fractures in institutionalized patients. Furthermore, 400 IU (10 microg) per day in combination with 1000 mg calcium or 100 000 IU orally every fourth month without calcium reduces fracture risk in individuals over 65 years of age living at home. Yearly injections of vitamin D seem to have no effect on fracture risk probably because of reduced bioavailability. Simulation studies suggest that fortification of food cannot provide sufficient vitamin D to the elderly without exceeding present conventional safety levels for children. A combination of fortification and individual supplementation is proposed. It is argued that all official programmes should be evaluated scientifically. Epidemiological studies suggest that vitamin D insufficiency is related to a number of other disorders frequently observed among the elderly, such as breast, prostate and colon cancers, type 2 diabetes, and cardiovascular disorders including hypertension. However, apart from hypertension, causality has not been established through randomized intervention studies. It seems that 800 IU (20 microg) vitamin D per day in combination with calcium reduces systolic blood pressure in elderly women.
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PMID:Vitamin D and the elderly. 1658 25

Vitamin D deficiency predisposes individuals to type 1 and type 2 diabetes, and receptors for its activated form-1alpha,25-dihydroxyvitamin D3-have been identified in both beta cells and immune cells. Vitamin D deficiency has been shown to impair insulin synthesis and secretion in humans and in animal models of diabetes, suggesting a role in the development of type 2 diabetes. Furthermore, epidemiological studies suggest a link between vitamin D deficiency in early life and the later onset of type 1 diabetes. In some populations, type 1 diabetes is associated with certain polymorphisms within the vitamin D receptor gene. In studies in nonobese diabetic mice, pharmacological doses of 1alpha,25-dihydroxyvitamin D3, or its structural analogues, have been shown to delay the onset of diabetes, mainly through immune modulation. Vitamin D deficiency may, therefore, be involved in the pathogenesis of both forms of diabetes, and a better understanding of the mechanisms involved could lead to the development of preventive strategies.
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PMID:Vitamin D and diabetes. 1634 26

Diabetes mellitus is associated with various organ dysfunctions through hyperglycemia, insulin deficiency, or advanced glycation end products, which can also cause impaired calcium homeostasis such as the reductions of parathyroid hormone secretion, vitamin D receptor (VDR) number, and 25- (OH) vitamin D-1 alpha-hydroxylase activity in the parathyroid gland, intestine, and kidney, respectively. On the contrary, abnormal calcium homeostasis such as vitamin D deficiency/insensitivity and hyperparathyroidism can cause glucose intolerance or diabetes. Vitamin D deficiency/insensitivity induces type 2 diabetes through impaired insulin secretion involving VDR on pancreatic beta cells, as well as type 1 diabetes through the reduction in immuno-modulatory action of 1,25 (OH)(2) vitamin D. Primary hyperparathyroidism induces glucose intolerance via insulin resistance due to elevated intracellular calcium in the targeted organ of insulin.
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PMID:[Calcium homeostasis and diabetes mellitus]. 1688 34

Vitamin D is essential for the maintenance of good health. Its sources can be skin production and diet intake. Most humans depend on sunlight exposure (UVB 290-315 nm) to satisfy their requirements for vitamin D. Solar ultraviolet B photons are absorbed by the skin, leading to transformation of 7-dehydrocholesterol into vitamin D3 (cholecalciferol). Season, latitude, time of day, skin pigmentation, aging, sunscreen use, all influence the cutaneous production of vitamin D3. Vitamin D deficiency not only causes rickets among children but also precipitates and exacerbates osteoporosis among adults and causes the painful bone disease osteomalacia. Vitamin D deficiency has been associated with increased risk for other morbidities such as cardiovascular disease, type 1 and type 2 diabetes mellitus and cancer, especially of the colon and prostate. The prevalence of hypovitaminosis D is considerable even in low latitudes and should be taken into account in the evaluation of postmenopausal and male osteoporosis. Although severe vitamin D deficiency leading to rickets or osteomalacia is rare in Brazil, there is accumulating evidence of the frequent occurrence of subclinical vitamin D deficiency, especially in elderly people.
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PMID:Vitamin D deficiency: A global perspective. 1711 89

Vitamin D deficiency has been shown to alter insulin synthesis and secretion in both humans and animal models. It has been reported that vitamin D deficiency may predispose to glucose intolerance, altered insulin secretion and type 2 diabetes mellitus. Vitamin D replenishment improves glycaemia and insulin secretion in patients with type 2 diabetes with established hypovitaminosis D, thereby suggesting a role for vitamin D in the pathogenesis of type 2 diabetes mellitus. The presence of vitamin D receptors (VDR) and vitamin D-binding proteins (DBP) in pancreatic tissue and the relationship between certain allelic variations in the VDR and DBP genes with glucose tolerance and insulin secretion have further supported this hypothesis. The mechanism of action of vitamin D in type 2 diabetes is thought to be mediated not only through regulation of plasma calcium levels, which regulate insulin synthesis and secretion, but also through a direct action on pancreatic beta-cell function. Therefore, owing to its increasing relevance, this review focuses on the role of vitamin D in the pathogenesis of type 2 diabetes mellitus.
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PMID:Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. 1826 34

Insulin resistance (IR) and its associated metabolic derangements are known complications of advanced chronic kidney disease (CKD). The etiology of IR in CKD is multifactorial with likely contributions from vitamin D deficiency, obesity, metabolic acidosis, inflammation, and accumulation of 'uremic toxins' leading to acquired defects in the insulin-receptor signaling pathway. An important consequence in end-stage renal disease (ESRD) is its role in the pathogenesis of uremic protein energy wasting, a commonly observed state of metabolic derangement characterized by loss of somatic and visceral protein stores not entirely accounted for by inadequate nutrient intake. In the general population, IR has been associated with accelerated protein catabolism. Among ESRD patients, enhanced muscle protein breakdown has been observed in patients with type 2 diabetes mellitus (DM) compared to ESRD patients without DM. In the absence of DM or severe obesity, IR is detectable in dialysis patients and strongly associated with increased muscle protein breakdown, even after controlling for inflammation. This process appears to be mediated by the ubiquitin-proteasome pathway. Given the high prevalence of protein energy wasting in ESRD and its unequivocal association with adverse clinical outcomes, IR may represent an important modifiable target for intervention in the ESRD population.
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PMID:Determinants of insulin resistance and its effects on protein metabolism in patients with advanced chronic kidney disease. 1845 70

Studies from our center and other parts of India have drawn attention towards wide prevalence of vitamin D deficiency (VDD) in our country. VDD has been reported in all age groups including toddlers, school children, pregnant women and their neonates and adult males and females residing in rural and urban India. We reviewed implications of VDD in our population based on the preliminary data available from Indian studies on skeletal health. Besides, a brief review is made on the importance of VDD in various other disorders prevalent in equivalent proportions among Indians such as type 2 diabetes mellitus (DM), cardiovascular diseases (CVD), immune competence including relation to tuberculosis, malignancy and osteoarthritis. Data from the West have also associated VDD with increased prevalence of type 2DM, CVD, autoimmune disorders, tuberculosis, prostate, breast and colon malignancy and osteoarthritis. Such association has not been studied to date in our country. Overall results of various studies conducted to date in urban and rural Indians indicate that widely prevalent VDD is functionally relevant to skeletal health including osteomalacia and rickets. However, there is a need to explore its association with osteoporosis related fractures and various other non skeletal disorders linked with VDD.
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PMID:Prevalence & potential significance of vitamin D deficiency in Asian Indians. 1849 36

Serum vitamin D has recently been inversely associated with risk for type 2 diabetes. Recent literature suggests that many more individuals than generally thought suffer from vitamin D deficiency. Southeast Alaskan Natives are at an increased risk due to limited sunlight exposure and possible inadequate vitamin D intake. Therefore, the relationship between vitamin D and glucose should be investigated specifically in the southeast Alaska Native population. A review of lab records yielded 83 charts of patients found to have a serum 25-hydroxyvitamin D during a 2-year period. Upon review of these charts, only nine of 83 vitamin D levels were found to exceed the 32 ng/mL (80 nmol/L) threshold. Age and vitamin D levels were associated in a positive linear relationship (r=0.354, P=0.028). The patients in the lowest vitamin D quartile were younger in age compared to the highest quartile (14.6 years, 95% confidence interval: 4.9, 24.29; P=0.004). The high rate of deficiency noted in this sample suggests this population should be further assessed for vitamin D deficiency. Future studies are needed to confirm the association between a vitamin D deficiency and diabetes incidence in this population.
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PMID:Vitamin D deficiency in a nonrandom sample of southeast Alaska Natives. 1875 24


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