Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D receptor (VDR) polymorphism influences susceptibility to type 1 diabetes, but the association with type 2 diabetes is not clear. We investigated the association between VDR polymorphism and type 2 diabetes and metabolic syndrome in a community-based study of unrelated older adults without known diabetes. Oral glucose tolerance test (75 g), plasma glucose and insulin measurement, homeostasis model assessment (HOMA), and VDR genotyping were performed. The distributions of genotype frequencies of ApaI, BsmI, and TaqI polymorphism did not differ between persons with and without diabetes, but the frequency of aa genotype of ApaI polymorphism was marginally higher in persons with type 2 diabetes (P =.058). Fasting plasma glucose (P <.05) and prevalence of glucose intolerance (P <.05) were significantly higher in nondiabetic persons with aa genotype compared with those with AA genotype. The bb genotype of BsmI polymorphism was associated with insulin resistance as assessed by HOMA after adjustment for age, sex, body mass index (BMI), and calcium and vitamin D use in persons without diabetes (P <.05). Our research suggests that ApaI polymorphism may be associated with glucose intolerance independent of defective insulin secretion and BsmI polymorphism with insulin resistance in a nondiabetic Caucasian population.
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PMID:Association between vitamin D receptor polymorphism and type 2 diabetes or metabolic syndrome in community-dwelling older adults: the Rancho Bernardo Study. 1237 Aug 62

The metabolic syndrome of chronic critical illness (CCI) consists of multisystem organ dysfunction resulting from the initial acute injury and chronic immune-neuroendocrine axis activation, adult kwashiorkor-like malnutrition, and prolonged immobilization with suppression of the PTH-vitamin D axis and hyper-resorptive metabolic bone disease. CCI patients can also present unique challenges in the management of diabetes mellitus, thyroid and adrenal diseases, electrolyte abnormalities and hypogonadism.
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PMID:Endocrine and metabolic issues in the management of the chronically critically ill patient. 1214 Sep 16

There is evidence from both observational studies and clinical trials that calcium malnutrition and hypovitaminosis D are predisposing conditions for various common chronic diseases. In addition to skeletal disorders, calcium and vitamin D deficits increase the risk of malignancies, particularly of colon, breast and prostate gland, of chronic inflammatory and autoimmune diseases (e.g. insulin-dependent diabetes mellitus, inflammatory bowel disease, multiple sclerosis), as well as of metabolic disorders (metabolic syndrome, hypertension). The aim of the present review was to provide improved understanding of the molecular and cellular processes by which deficits in calcium and vitamin D cause specific changes in cell and organ functions and thereby increase the risk for chronic diseases of different aetiology. 1,25-Dihydroxyvitamin D(3) and extracellular Ca(++) are both key regulators of proliferation, differentiation and function at the cellular level. However, the efficiency of vitamin D receptor-mediated intracellular signalling is limited by the negative effects of hypovitaminosis D on extrarenal 25-hydroxyvitamin D-1alpha-hydroxylase activity and thus on the production of 1,25-dihydroxyvitamin D(3). Calcium malnutrition eventually causes a decrease in calcium concentration in extracellular fluid compartments, resulting in organ-specific modulation of calcium-sensing receptor activity. Hence, attenuation of signal transduction from the ligand-activated vitamin D receptor and calcium-sensing receptor seems to be the prime mechanism by which calcium and vitamin D insufficiencies cause perturbation of cellular functions in bone, kidney, intestine, mammary and prostate glands, endocrine pancreas, vascular endothelium, and, importantly, in the immune system. The wide range of diseases associated with deficits in calcium and vitamin D in combination with the high prevalence of these conditions represents a special challenge for preventive medicine.
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PMID:Vitamin D and calcium deficits predispose for multiple chronic diseases. 1586 41

Early feeding may modify the risk of both type 1 (T1D) and type 2 diabetes (T2D) later in life. The information generated so far is, however, controversial. When evaluating studies on the impact of early feeding on risk of later diabetes, the data have to be assessed critically and possible confounding factors have to be considered. The study design may induce biases and there are considerable differences in early feeding practices across various countries and cultures. Accordingly it may not be possible to generalise observations based on one population. Long breastfeeding, exclusive breastfeeding in particular, and supplementation with vitamin D in infancy have been reported to confer partial protection against beta-cell autoimmunity and TID. In contrast, early exposure to cow's milk proteins and cereals and heavy weight in infancy have been implicated as risk factors for T1D. Long breastfeeding has also been observed to protect against T2D in aboriginal populations. Poor fetal nutrition resulting in low birth weight has been identified as a factor contributing to later insulin resistance and T2D. Recent data indicate that current overweight and obesity are stronger determinants of insulin resistance than birth weight among preschool children. High-nutrient diet and rapid growth in early infancy have been reported to adversely programme the principal components of the metabolic syndrome including insulin resistance and T2D. It is an important scientific and public-health objective to define protective and predisposing effects of early nutrition on the development of diabetes, since early feeding can potentially be modified to minimise the risk of later chronic diseases.
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PMID:Early nutrition and later diabetes risk. 1613 19

Previous research has reported reduced serum 25-hydroxyvitamin D levels in patients with chronic kidney disease (CKD), although the relationship between vitamin D status and insulin resistance (IR) in patients with CKD has not been examined in the general population. We examined the association that kidney function, based on glomerular filtration rate (eGFR) estimated from serum creatinine, has with serum levels of 25-hydroxyvitamin D and components of the metabolic syndrome among 14 679 participants in the Third National Health and Nutrition Examination Survey (NHANES III). In this analysis, adjusted mean serum 25-hydroxyvitamin D was significantly lower only in the participants with a severe (15-29 ml/min/1.73 m(2)) decrease in eGFR compared to those with normal kidney function (61.6 vs 73.3 nmol/l, P=0.0063). Serum 25-hydroxyvitamnin D (P=0.0018) and level of kidney function (P=0.0003) were inversely associated, independent of each other, with homeostasis model assessment of insulin resistance (HOMA-IR), adjusting for confounders. Participants with high 25-hydroxyvitamin D levels (>81 nmol/l) had lower HOMA-IR. We conclude that 25-hydroxyvitamin D deficiency is not as prevalent in the US general population with decreased eGFR as previously reported in patients with CKD; and that vitamin D and kidney function have independent inverse associations with IR.
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PMID:25-Hydroxyvitamin D, insulin resistance, and kidney function in the Third National Health and Nutrition Examination Survey. 1819 97

The identification of vitamin D receptor expression in different tissues suggests a widespread role for vitamin D action beyond its classical function in bone and mineral metabolism. Recently, the importance of vitamin D status as a risk factor in the development of metabolic syndrome has been the focus of several studies.
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PMID:Vitamin D status and the metabolic syndrome. 1713 43

Many factors are involved in infants' health; one of the most important of them may be the kind of early feeding. Recent evidences suggest that breastfeeding, in addition to its well-established beneficial effects during lactation period, provides also beneficial long-term effects, like the protection against infectious and immune-related diseases, a better cognitive development, a decreased risk of metabolic syndrome and of obesity. It has been reported that the early feeding mode affects growth and body composition and it could be considered a critical factor for metabolic development. Human milk is a source of different nutrients and bioactive factors, especially hormones and growth factors like leptin, ghrelin, insulin, insulin-like growth factor (IGF-I) playing a role in food intake regulation, metabolism and body composition. In particular breast milk leptin may provide a physiological explanation for a number of advantages seen in reaching proper growth and energy balance in breast-fed infants compared with formula fed ones. Etiopathogenesis and therapeutic approach in common minor gastrointestinal diseases in infants are important subject of study for pediatricians. Colic, constipation and regurgitation can be considered feeding problems and they might benefit from dietary treatment. Regarding infantile colic, dietary modifications seem to be more suitable than pharmacological treatment in resolving symptoms; also prebiotics and probiotics are useful for this aim. The occurence of constipation is related to the kind of feeding and it is lower in breastfed infants. Moreover formulas with probiotics and beta-palmitic acid could promote a regression of symptoms. A dietary approach may be useful also in regurgitation. Anyway we have to remember that breastfeeding require a supplementation of vitamin D and K for some months and a correct weaning program is needed from the 5th-6th months of life to prevent iron deficiency.
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PMID:[Breast milk: biological constituents for health and well-being in infancy]. 1726 42

Nuclear receptors are ligand-inducible transcriptional factors, and regulate various significant biological phenomena such as cell differentiation, proliferation, metabolism, and homeostasis. By the elucidation of the physiological functions of nuclear receptors, they have become one of the most significant molecular targets for drug discovery in the fields of cancer, autoimmune diseases, and metabolic syndrome. In this study, several novel nuclear receptor ligands have been developed, based on the receptor-folding inhibition hypothesis is discussed. In this hypothesis, the antagonists for nuclear receptors are classified into two types, the misfolding inducers and the folding inhibitors, related to the helix 12 (AF-2 region) conformation of the receptor that is significant for the receptor activation. Then, in order to overcome the resistance in the treatment of prostate tumors with androgen antagonists, the novel folding-inhibitor type antagonists such as isoxazole and pyrrolecarboxamide derivatives were designed and synthesized. Some of them exhibited the androgen antagonistic activities in LNCaP cells with mutated androgen receptor in which conventional antagonists such as flutamide and RU56187 were inactive. The folding-inhibitor type vitamin D3 antagonists (DLAM series) are similarly developed. Further, novel non-seco-steroidal vitamin D3 analogs were designed and synthesized by using a 3,3-diphenylpropane derivative, LG190178 as lead compound. The aza analogs exhibited both potent vitamin D agonistic and androgen antagonistic activities. The results indicate the drug design based on the receptor-folding inhibition hypothesis is efficient in medicinal chemistry of nuclear receptors.
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PMID:[Development of novel nuclear receptor ligands based on receptor-folding inhibition hypothesis]. 1726 54

The metabolic syndrome (MetS) is a clustering of metabolic abnormalities that increase the risk of developing atherosclerotic cardiovascular disease and type 2 diabetes. The exact etiology remains unclear, but it is known to be a complex interaction between genetic, metabolic, and environmental factors. Among environmental factors, dietary habits are of central importance in the prevention and treatment of this condition. However, there is currently no firm consensus on the most appropriate dietary recommendations. General recommendations include decreasing obesity, increasing physical activity, and consuming an anti-atherogenic diet, and have traditionally focused on low total fat intake. A major problem with the focus on low fat is that high-carbohydrate diets can contribute to increasing triglyceride and decreasing high-density lipoprotein (HDL) concentrations. Low-carbohydrate diets have been popular in recent years. However, such diets are typically higher in saturated fat and lower in fruits, vegetables, and whole grains than national dietary recommendations. More recently the quality of carbohydrate has been studied in relation to MetS, including a focus on dietary fiber and glycemic index. Similarly, there has been a move from limiting total fat to a focus on the quality of the fat, with evidence of beneficial effects of replacing some carbohydrate with monounsaturated fat. Other nutrients examined for possible importance include calcium, vitamin D, and magnesium. Together, the evidence suggests that the components of diet currently recommended as "healthy" are likely also protective against MetS, including low saturated and trans fat (rather than low total fat) and balanced carbohydrate intake rich in dietary fiber, as well as high fruit and vegetable intake (rather than low total carbohydrate); and the inclusion of low-fat dairy foods. Accelerating research on gene-diet interactions is likely to contribute interesting information that may lead to further individualized dietary guidance in the future.
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PMID:Nutritional strategies in the prevention and treatment of metabolic syndrome. 1733 84

Vitamin D deficiency is a risk factor for osteoporosis and other chronic diseases, including type 1 diabetes, hypertension, metabolic syndrome, and ischemic heart disease. Cholesterol and vitamin D share the 7-dehydrocholesterol metabolic pathway. This study evaluated the possible effect of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Eighty-three patients (52 men and 31 women) with an acute coronary syndrome (75 with acute myocardial infarction and 8 with unstable angina) were included. After diagnosis, patients received atorvastatin as secondary prevention. Serum vitamin D was measured by high-performance liquid chromatography at baseline and at 12 months. Atorvastatin treatment produced a statistically significant decrease in cholesterol and triglyceride levels and an increase in vitamin D levels (41+/-19 vs 47+/-19 nmol/L, p=0.003). Vitamin D deficiency was decreased by 75% to 57% at 12 months. In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels.
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PMID:Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. 1792 Mar 83


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