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 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of adipose tissue in health as well as disease has been demonstrated in several studies recently, and it has become appropriate to use the term 'adipose organ' when referring to adipose tissue as a whole. The obesity epidemic, with a marked increase in the incidence of the metabolic syndrome leading to diabetes type 2 as well as cardiovascular complications, has stimulated considerable interest in adipose tissue biology. Moreover, several studies in different species have shown that limited energy intake is associated with less inflammation, improved biomarkers of health and a marked increase in longevity. In addition, there is convincing evidence that an optimal amount of adipose tissue is essential for many body functions such as immune response, reproduction and bone quality. Some nutrients and their metabolites are important as energy sources as well as ligands for many transcription factors expressed in adipose tissue, including all energy-providing nutrients both directly and indirectly as well as cholesterol, vitamin E and vitamin D. In particular, fatty acids can be effectively taken up by adipocytes and they can interact with several transcription factors crucial for growth, development and metabolic response, e.g. PPARalpha, -delta and -gamma, sterol regulatory element-binding proteins1 and 2 and liver X receptors alpha and beta). Moreover, glucose is also readily taken up and stored as fatty acids via lipogenesis in adipocytes. It is known that some metabolic signals released as proteins from adipose tissue (adipokines) are important for normal as well as pathological responses to the amount of energy stored in the adipose organ. The future challenge will be to understand the function of adipose tissue in energy homeostasis and the interplay with nutrients in order to be able to give optimal advice for the prevention and treatment of obesity.
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PMID:The interplay between nutrients and the adipose tissue. 1746

Insulin resistance is characterized by the systemic impairment of insulin action and is usually the result of aging, obesity, chronic inflammation, or another factor that may contribute to the inhibition of the insulin signaling pathway. Insulin resistance is accompanied by defects in lipid metabolism and blood coagulation, hypertension, obesity, and vascular inflammation in a syndrome called syndrome X or metabolic syndrome. Metabolic syndrome is involved in the development of atherosclerosis with consequent cardiovascular complications including acute myocardial infarction, stroke, and vascular disease. Recent data have shown that vitamin D acts as a negative regulator of the renin gene and that vitamin D deficiency is followed by increased renin-angiotensin II expression. The link between the insulin signaling pathway/insulin resistance and the renin-angiotensin system has been well documented in previous studies. The present review focuses on disorders characterized by a reduction in vitamin D concentration or its receptor function and the development of insulin resistance or metabolic syndrome, and discusses also possible therapeutic interventions.
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PMID:Vitamin D, the renin-angiotensin system, and insulin resistance. 1819 90

Hyperglycemia and increase in advanced glycation end products in patients with diabetes are known to cause impaired calcium homeostasis such as reduction in parathyroid hormone secretion, decrease in calcium (Ca) absorption resulting from impaired vitamin D action, increase in urinary Ca excretion, impaired osteoblastic function, and deterioration of bone quality. On the other hand, fat deposition accompanied by the metabolic syndrome are positively linked to increased bone mineral density (BMD) and reduced fracture risk through increased body weight. However, body fat has a detrimental effect on BMD after adjustment for weight, and gives less mechanical stress on bone than muscle tissue that is firmly attached to bone via the tendon. Thus, converting fat into muscle tissue by regular exercise and healthy diet helps not only prevent hyperglycemia but also osteoporosis.
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PMID:[Calcium homeostasis and osteoporosis in diabetes mellitus and the metabolic syndrome]. 1859 40

Common obesity is associated with the metabolic syndrome and can be distinguished from secondary obesity and from rare forms of monogenic and polygenic obesity. The prevalence of common obesity has become a public health concern in many countries as phenomenological approaches to the understanding of obesity have failed to achieve any long term effect on prevention or treatment. There is evidence for a central control mechanism which maintains body-weight to a set-point by the regulation of energy intake and energy expenditure through homeostatic pathways. It is suggested in this paper that common obesity occurs when the set-point is raised and that accumulation of fat mass functions to increase body size. Larger body size confers a survival advantage in the cold ambient temperatures and food scarcity of the winter climate by reducing surface area to volume ratio and by providing an energy store in the form of fat mass. In addition, it is suggested that the phenotypic metabolic and physiological changes observed as the metabolic syndrome, including hypertension and insulin resistance, could result from a winter metabolism which increases thermogenic capacity. Common obesity and the metabolic syndrome may therefore result from an anomalous adaptive winter response. The stimulus for the winter response is proposed to be a fall in vitamin D. The synthesis of vitamin D is dependent upon the absorption of radiation in the ultraviolet-B range of sunlight. At ground level at mid-latitudes, UV-B radiation falls in the autumn and becomes negligible in winter. It has previously been proposed that vitamin D evolved in primitive organisms as a UV-B sensitive photoreceptor with the function of signaling changes in sunlight intensity. It is here proposed that a fall in vitamin D in the form of circulating calcidiol is the stimulus for the winter response, which consists of an accumulation of fat mass (obesity) and the induction of a winter metabolism (the metabolic syndrome). Vitamin D deficiency can account for the secular trends in the prevalence of obesity and for individual differences in its onset and severity. It may be possible to reverse the increasing prevalence of obesity by improving vitamin D status.
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PMID:Vitamin D deficiency is the cause of common obesity. 1928 11

Diabetes is a leading cause of cardiovascular disease. Persons with diabetes are at greater risk for early cardiac mortality, and for repeat events if they survive their first cardiac event. Recently, low serum concentrations of vitamin D have been associated with increased risk for cardiac events. Evidence indicates that persons with diabetes have lower serum concentrations of vitamin D. In addition, persons at risk for diabetes or metabolic syndrome have inadequate serum concentrations of vitamin D. This review will assess the evidence relative to the impact of vitamin D in the development of diabetes, metabolic syndrome, and diabetes complications. Studies that address vitamin D and its impact on metabolic outcomes as well as possible mechanisms of action are provided. Finally, the assessment and suggested treatment for vitamin D deficiency is addressed. Effective detection and treatment of inadequate vitamin D concentrations in persons with diabetes or those at risk for diabetes may be an easy and cost-effective therapy which could improve their long-term health outcomes as well as their quality of life.
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PMID:Vitamin D and diabetes: let the sunshine in. 1907 78

Evaluation of: Knekt P, Laaksonen M, Mattila C et al.: Serum vitamin D and subsequent occurrence of Type 2 diabetes. Epidemiology 19, 666-671 (2008). Cross-sectional studies have demonstrated that lower serum 25-hydroxyvitamin D (25[OH]D) levels are associated with obesity, the metabolic syndrome, impaired glucose tolerance and diabetes. However, as in all cross-sectional studies, the direction of causation is unclear. The article by Knekt et al. was the first prospective study to demonstrate that low 25(OH)D levels predict incident diabetes. This study utilized a nested case-control design of 412 incident diabetes cases and 986 age/sex matched controls drawn from two large Finnish cohorts totaling 7503 participants aged 40 years and over followed for up to 22 years. In men, although not in women, higher baseline 25(OH)D reduced the risk of incident diabetes by 72%. Recently, other prospective cohort studies have shown that baseline 25(OH)D deficiency is associated with incident cardiovascular disease events and mortality over follow-up, a relationship that may be mediated, in part, through incident diabetes. While animal studies and smaller interventional trials in humans suggest that vitamin D supplementation improves measures of insulin sensitivity and glucose tolerance, larger interventional trials are warranted to determine if vitamin D treatment at adequate doses can prevent diabetes.
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PMID:Vitamin D deficiency and the risk of incident Type 2 diabetes. 1849 68

A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1 alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) and extracellular Ca(2+) act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)(2)D(3)-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.
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PMID:Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. 1972 93

Recent research has implicated vitamin D deficiency (serum levels of 25-hydroxyvitamin D <50 nmol/L) with a number of chronic conditions, including autoimmune conditions such as multiple sclerosis, lupus, and psoriasis, and chronic conditions such as osteoporosis, osteoarthritis, metabolic syndrome, fibromyalgia and chronic fatigue syndrome. It has been assumed that low levels of 25-hydroxyvitamin D (25-D) accurately indicate vitamin D storage and vitamin D receptor (VDR)-mediated control of calcium metabolism and innate immunity. To evaluate this assumption, 25-D and 1,25-dihydroxyvitamin D3 (1,25-D) levels were measured in 100 Canadian patients with these conditions. Additionally, other inflammatory markers (CK, CRP) were measured. Results showed a strong positive association between these autoimmune conditions and levels of 1,25-D >110 pmol/L. However, there was little association with vitamin D deficiency or the other inflammatory markers, meaning that the results challenge the assumption that serum levels of 25-D are a sensitive measure of the autoimmune disease state. Rather, these findings support the use of 1,25-D as a clinical marker in autoimmune conditions. High levels of 1,25-D may result when dysregulation of the VDR by bacterial ligands prevents the receptor from expressing enzymes necessary to keep 1,25-D in a normal range.
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PMID:Vitamin D metabolites as clinical markers in autoimmune and chronic disease. 1975 77

Lifestyle factors predict type 2 diabetes occurrence, but their effect in high- and low-risk populations is poorly known. This study determines the prediction of low-risk lifestyle on type 2 diabetes in those with and without metabolic syndrome in a pooled sample of two representative Finnish cohorts, collected in 1978-1980 and 2000-2001. Altogether 8,627 individuals, aged 40-79 years, and free of diabetes and cardiovascular disease at baseline were included in this study. A low-risk lifestyle was defined based on body mass index, exercise, alcohol consumption, smoking, and serum vitamin D concentration. The metabolic syndrome was defined according to the International Diabetes Federation including obesity, blood pressure, serum HDL cholesterol, serum triglycerides, and fasting glucose. During a 10-year follow-up, altogether 226 type 2 diabetes cases occurred. Overweight was the strongest predictor of type 2 diabetes (population attributable fraction (PAF) = 77%, 95% confidence interval (CI): 53, 88%). Together with lack of exercise, unsatisfactory alcohol consumption, smoking, and low vitamin D concentration it explained 82% of the cases. Altogether 62% (CI: 47, 73%) of the cases were attributable to the metabolic syndrome and 92% (CI: 67, 98%) to the most unfavourable combination of its components. The metabolic syndrome did not modify the prediction of lifestyle factors but persons with normal blood pressure benefited more from positive changes in exercise, alcohol consumption, and smoking than those with elevated blood pressure (P for interaction = 0.01). In conclusion, modification of lifestyle factors apparently reduces type 2 diabetes risk, especially in persons with normal blood pressure.
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PMID:The relative importance of modifiable potential risk factors of type 2 diabetes: a meta-analysis of two cohorts. 2001 85

Cardiometabolic disorders and vitamin D deficiency are becoming increasingly more prevalent across multiple populations. Different studies have suggested a potential association between abnormal vitamin D levels and multiple pathological conditions including cardiovascular diseases and diabetes. We aimed to evaluate the association between vitamin D levels, using 25-hydroxy vitamin D (25OHD) as an indicator of vitamin D status, and the presence of cardiometabolic disorders including cardiovascular disease, diabetes and metabolic syndrome. We performed a systematic review of the current literature on vitamin D and cardiometabolic disorders using the PubMed and Web of Knowledge databases in September 2009. Studies in adults looking at the effect of vitamin D levels on outcomes relating to cardiometabolic disorders were selected. We performed a meta-analysis to assess the risk of developing cardiometabolic disorders comparing the highest and lowest groups of serum 25OHD. From 6130 references we identified 28 studies that met our inclusion criteria, including 99,745 participants. There was moderate variation between the studies in their grouping of 25OHD levels, design and analytical approach. We found that the highest levels of serum 25OHD were associated with a 43% reduction in cardiometabolic disorders [OR 0.57, 95% (CI 0.48-0.68)]. Similar levels were observed, irrespective of the individual cardiometabolic outcome evaluated or study design. High levels of vitamin D among middle-age and elderly populations are associated with a substantial decrease in cardiovascular disease, type 2 diabetes and metabolic syndrome. If the relationship proves to be causal, interventions targeting vitamin D deficiency in adult populations could potentially slow the current epidemics of cardiometabolic disorders.
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PMID:Levels of vitamin D and cardiometabolic disorders: systematic review and meta-analysis. 2003 48


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