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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interactions of serum levels of magnesium and parathyroid hormone (PTH) have been studied in a patient with hypomagnesemia and hypocalcemia following intestinal bypass surgery for obesity. When serum magnesium was low serum PTH was not stimulated by hypocalcemia. With correction of magnesium deficiency hypocalcemia was associated with elevation of serum PTH levels. Infusion of exogenous PTH induced a clearly detectable renal response in the presence of hypomagnesemia but the response was diminished when serum magnesium was elevated. In this patient it appears that hypomagnesemia suppressed parathyroid gland activity, leaving the renal action of PTH intact.
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PMID:Influence of magnesium on the secretion and action of parathyroid hormone. 23 Oct 63

Obesity is characterized by a high risk for glucose intolerance and cardiovascular disease. Since magnesium deficiency or depletion have often been associated with both pathologies, is of interest to study magnesium status in severely obese subjects before any form of treatment. Negative magnesium balances have been described in overweight persons submitted to total starvation, hypocaloric diets, and obesity surgery. For this reason 80 non-diabetic obese men and 118 age-matched obese women were studied. Serum and erythrocyte magnesium concentrations were significantly higher in the male population but the mean values were not suggestive of a magnesium deficit before any form of treatment was started. Since metabolic abnormalities and cardiovascular risk are greater in patients with upper body fat distribution (UBFD) both sexes were subdivided according to "waist-to-hip" circumference ratio. No difference could be shown in the obese men but in women, UBFD subjects showed higher basal insulin levels and increased erythrocyte magnesium concentration as compared to those with classical gynoid fat distribution. A 75 g oral glucose tolerance test enabled the subjects to be subdivided into those with normal or impaired glucose tolerance (IGT). The IGT group in both sexes was older and more obese. Mean values of serum magnesium and erythrocyte magnesium were not decreased despite the more pronounced insulin resistance in the IGT group. However a significant negative correlation was found between fasting blood sugar/insulinaemia and erythrocyte magnesium, showing that this middle-aged obese population can maintain normal circulating levels of magnesium, in contrast to type II diabetics or older subjects where for other reasons (urinary losses or decreased intake) magnesium status is interfered with.
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PMID:Magnesium and obesity: influence of gender, glucose tolerance, and body fat distribution on circulating magnesium concentrations. 146 56

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.
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PMID:Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet. 183 14

The concentration of magnesium in muscle was determined and a standardized magnesium load test was performed in 21 patients, who 4 to 10 years previously had undergone intestinal bypass operations for severe obesity. The plasma concentration and 24-h urinary excretion of magnesium were also studied. Basic urinary excretion of magnesium and muscle magnesium were significantly lower in patients compared to healthy controls, while no differences were found in plasma magnesium. A slight negative correlation between muscle magnesium and retained magnesium was demonstrated (r = -0.51, P less than 0.05). Patients with magnesium retention greater than 20 per cent showed a significant decrease of magnesium retention after treatment with magnesium chloride mixture. Four patients with primarily low muscle magnesium all demonstrated an increment in the amount of magnesium in muscle after treatment. The load test described can be applied as a screening test in diagnosing magnesium deficiency.
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PMID:A magnesium load test in the diagnosis of magnesium deficiency. 362 92

Improving the action of insulin is a relatively new concept in therapy. It should, however, become more and more important because of the rapid expansion of the insulin resistance syndrome (including upper body adiposity, glucose intolerance, hypertension, dyslipidaemia, etc.) in industrialized countries and its dramatic consequences for public health. Insulin sensitivity can be improved by non-pharmacological means, essentially reduction of excessive body weight, promotion of regular physical activity and modification of dietary habits, as well as, possibly, cessation of smoking and correction of subclinical magnesium deficiency. Currently available pharmacological means mainly include the biguanide compound metformin and possibly anti-obesity agents, such as (d-) fenfluramine, fluoxetine and benfluorex. New compounds aiming at improving the action of insulin are in development, especially the thiazolidinedione derivatives (e.g. troglitazone), known as 'insulin sensitizers'. Treatment of insulin resistance may have important gynaecological applications, essentially in polycystic ovary syndrome and, possibly, after menopause. Hopefully, improving insulin sensitivity could ameliorate the cardiovascular prognosis of numerous individuals having some or all components of insulin resistance syndrome.
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PMID:Perspective in the treatment of insulin resistance. 940 22

The clinical and public health impact of the metabolic syndrome (MetS) has increased substantially in recent years. MetS is defined by a constellation of cardiovascular disease risk factors including: insulin resistance, elevated blood pressure, impaired glucose tolerance, central obesity, and atherogenic dyslipidemia as well as impaired clotting, increased inflammatory burden, and oxidative stress. Recently, there has been burgeoning experimental, clinical, and epidemiological data that provides strong evidence that dietary magnesium intake and supplementation are inversely associated with the risk for MetS and its components. In this review, we describe and discuss the myriad of integrated physiological mechanisms through which magnesium deficiency and the resultant altered magnesium status may lead to the development of the MetS and each of its components.
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PMID:Magnesium physiology and pathogenic mechanisms that contribute to the development of the metabolic syndrome. 1806 85

The review concerning a value of magnesium in an organism in healthy persons and cases with endocrine disorders is presented. The causes of magnesium-deficient conditions in cases with type 1 and type 2 diabetes, thyrotoxic goiter, hypothyroidism and obesity were analyzed. Participation of magnesium in secretion of parathormone and a control of calcium exchange is shown. The clinical semiology of hypomagnesemia seems to be nonspecific and manifold, and, therefore, as a rule, in most of endocrine patients magnesium deficiency remains to be undiagnosed. Questions on preventive measures and management of treatment magnesium-deficient conditions are considered.
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PMID:[Magnesium deficiency in an endocrinologist's practice]. 1875 48

Along with the growing epidemic of obesity, the risk of atherosclerosis, cardiovascular disease morbidity, and mortality are increasing markedly. Several risk factors for cardiovascular disease, such as visceral obesity, glucose intolerance, arterial hypertension, and dyslipidemia commonly cluster together as a condition currently known as metabolic syndrome. Thus far, insulin resistance, and endothelial dysfunction are the primary events of the metabolic syndrome. Several groups have recommended clinical criteria for the diagnosis of metabolic syndrome in adults. Nonetheless, in what concerns children and adolescents, there are no unified definitions, and modified adult criteria have been suggested by many authors, despite major problems. Some pediatric disease states are at risk for premature cardiovascular disease, with clinical coronary events occurring very early in adult life. Survivors of specific pediatric cancer groups, particularly acute lymphocytic leukemia, central nervous system tumors, sarcomas, lymphomas, testicular cancer, and following bone marrow transplantation, may develop metabolic syndrome traits due to: hormonal deficiencies (growth hormone deficiency, thyroid dysfunction, and gonadal failure), drug or radiotherapy damage, endothelial impairment, physical inactivity, adipose tissue dysfunction, and/or drug-induced magnesium deficiency. In conclusion, some primary and secondary prevention remarks are proposed in order to reduce premature cardiovascular disease risk in this particular group of patients.
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PMID:Detection of metabolic syndrome features among childhood cancer survivors: a target to prevent disease. 1906 99

About 60% of adults in the United States do not consume the estimated average requirement for magnesium, but widespread pathological conditions attributed to magnesium deficiency have not been reported. Nevertheless, low magnesium status has been associated with numerous pathological conditions characterized as having a chronic inflammatory stress component. In humans, deficient magnesium intakes are mostly marginal to moderate (approximately 50% to <100% of the recommended dietary allowance). Animal experiments indicate that signs of marginal-to-moderate magnesium deficiency can be compensated or exacerbated by other factors influencing inflammatory and oxidative stress; recent studies suggest a similar happening in humans. This suggestion may have significance in obesity, which is characterized as having a chronic low-grade inflammation component and an increased incidence of a low magnesium status. Marginal-to-moderate magnesium deficiency through exacerbating chronic inflammatory stress may be contributing significantly to the occurrence of chronic diseases such as atherosclerosis, hypertension, osteoporosis, diabetes mellitus, and cancer.
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PMID:Magnesium, inflammation, and obesity in chronic disease. 2053 78

Chronic exposure to insufficient levels of magnesium (Mg) in drinking water increases the risk of magnesium deficiency and its association with hypertension, dyslipidemia and type 2 diabetes mellitus. The aim of the study was to assess the potential association of mineral contents in drinking water with blood pressure and other components of metabolic syndrome (MetS) (BMI as measure of obesity, triglycerides, glucose, and insulin resistance, index-HOMA IR), in a healthy population. This study was conducted in three randomly selected municipalities (Pozarevac, Grocka and Banovci), and recruited 90 healthy blood donors, aged 20-50 years. The Pozarevac area had a four times higher mean Mg level in drinking water (42 mg L(-1)) than Grocka (11 mg L(-1)). Diastolic blood pressure was lowest in subjects from Pozarevac. Serum Mg (sMg) was highest, and serum Ca(2+)/Mg (sCa/Mg) lowest in subjects from Pozarevac, and after adjustment for confounders (age, gender, BMI), only total cholesterol and sMg levels were independent predictors of diastolic blood pressure, sMg levels were independent predictors of triglycerides, and sCa/Mg predicted glucose levels. These results suggest that Mg supplementation in areas of lower magnesium levels in drinking water may be an important measure in the prevention of hypertension and MetS in general.
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PMID:Association of blood pressure and metabolic syndrome components with magnesium levels in drinking water in some Serbian municipalities. 2236 11


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