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

Calcium and magnesium balance, 47Ca turnover studies, and measurements of vitamin D metabolites were performed before and after 7-10 months of vitamin D2 treatment (36,000 IU/day) in eight patients bypass-operated 3-6 years earlier for gross obesity. All patients had received a daily supplementation of calcium (27 mmol/day) since operation. Before treatment the net calcium absorption and calcium balance were normal compared with that of nine normal controls. Vitamin D metabolites were within normal limits. The endogenous faecal calcium level was increased and the faecal lag time shortened. Bone biopsies revealed osteomalacia in three of the patients. Vitamin D2 treatment induced an increase in calcium absorption and renal excretion of calcium, a reduced bone resorption rate, a more positive calcium balance, and healing of osteomalacia. Moreover, the vitamin D2 treatment induced a prolongation and normalization of faecal lag time, an increase in magnesium absorption, and a more positive magnesium balance. The effect might be mediated through 25-hydroxyvitamin D (25-OHD), which increased, whereas serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D) and 24,25-dihydroxyvitamin D (24,25-(OH)2D) were unchanged. The results indicate that in some bypass-operated patients high-dose vitamin D2 has a beneficial effect on calcium and magnesium metabolism.
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PMID:Treatment with high-dose oral vitamin D2 in patients with jejunoileal bypass for morbid obesity. Effects on calcium and magnesium metabolism, vitamin D metabolites, and faecal lag time. 633 25

17 beta-Estradiol (E2) pellet replacement therapy for oophorectomized women has been shown to be safe and effective. Some investigators have advocated the addition of testosterone (T) pellets for oophorectomized women. This study was carried out to measure the level of androgens in oophorectomized women with and without E2 pellets. The possible modulating role of E2 upon adrenal androgens was investigated as well as the effects of obesity on bound and unbound serum levels of E2 and T. Seven obese patients and eight nonobese normal patients with E2 pellets were compared to nine oophorectomized age- and weight-matched control women not receiving estrogen. Obese patients had higher levels of androstenediol (Adiol) and androstenedione (A) than nonobese patients, yet compared to oophorectomized controls, nonobese patients had higher levels of dehydroepiandrosterone sulfate (DHEA-S) and Adiol. As a group, patients with E2 pellets had higher levels of DHEA-S, Adiol A, and unbound T compared to oophorectomized controls, and their Adiol and total and unbound T levels were similar to those of premenopausal females. Obese patients had lower levels of total E2, yet a higher percentage of unbound E2, resulting in unbound E2 levels which were similar to those of the nonobese women. Unbound T was higher in obese patients compared to the nonobese women and oophorectomized controls. In conclusion, these data suggest that 1) there may be a modulating role of E2 on adrenal androgens exemplified by an increased serum level of delta 5-3 beta-ol androgens in women with E2 pellets, 2) supplemental T implants for oophorectomized women may not be necessary, and 3) obese women with pellets have higher levels of Adiol, A, and unbound T then nonobese women and therefore have a higher ratio of androgen to estrogen.
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PMID:The modulating role of obesity and 17 beta-estradiol (E2) on bound and unbound E2 and adrenal androgens in oophorectomized women. 645 39

The influence of alimentary obesity on the functional morphology of the adrenal cortex and glandulocytes of the testis was studied in male Wistar rats with an initial weight of 60--70 g. Analysis of some of histochemical parameters during obesity showed the disturbance of the operating mode of adrenocorticocytes and glandulocytes which manifested by changes in the activity of 3 beta-ol-dehydrogenase, glucoso-6-phosphate dehydrogenase and NADP.H-diaphorases. It was also found that obese rats had the increased adrenoglucocorticoid activity.
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PMID:[Morphological characteristics of steroid-producing glands in alimentary obesity]. 694 28

The detection of clinical hyperandrogenism in women presenting with infertility requires detailed hormonal investigations using the decisional plan suggested here. Initial studies including measurement of plasma androgen, gonadotrophic hormones and prolactin levels, may be sufficient to reveal an adrenal origin or pure ovarian origin. Non-tumor androgenic hypercorticism is seen classically in late-presenting enzyme deficits, but also in other situations: excessive adrenarche, hyperprolactinemia, obesity, chronic stress. The immediate Synacthene test can then eliminate diagnostic uncertainties if it leads to the discovery of appearances of 21- or 11-hydroxylase or 3 beta-ol dehydrogenase blocks. Intense virilisation in a woman with a testosterone level above 2 ng/ml (7 nM/l) should lead to suspicion of an androgen-secreting tumor of the ovary or adrenal. CT scan of the abdomen and true pelvis is essential here since it may reveal the presence of an adrenal or ovarian mass. If no morphological abnormality is shown by this investigation, an endocrine lesion of a small ovary should be strongly suspected, the demonstration of which requires isotope techniques and/or catheterisation of the ovarian veins. Two situations also exist which are responsible for severe hyperandrogenism but less alarming in terms of their course and significance: certain homozygous forms of 21-hydroxylase deficit diagnosed late and ovarian hyperthecosis. It may happen that these hormonal investigations do not suffice alone to determine the precise origin of hyperandrogenism and its cause. The dexamethasone adrenal suppression test is useful in the diagnosis of type II micropolycystic dystrophy, in order to define the essentially ovarian, adrenal or mixed origin of hyperandrogenism.
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PMID:[Diagnostic strategy in infertility due to hyperandrogenism. Development of a decision tree]. 803 86

Orlistat, a potent gastrointestinal lipase inhibitor, is a member of a new class of drugs designed for the long-term treatment of obesity. When given with a fat-containing meal, orlistat reduces dietary fat absorption by approximately 30%, which equates to a decrease in caloric absorption of approximately 200 kilocalories per day. A 2-year European study found a mean decrease in body weight of 10.2% (10.3 kg) in the orlistat group compared to 6.1% (6.1 kg) in the placebo group at 1 year. Additionally, 9.3% of the orlistat group versus 2.1% of the placebo group lost >20% of their initial weight. Serum lipids and diabetes control are also improved by orlistat. Related to orlistat's mechanism of action, side effects include oily spotting, flatulence and frequent loose stools, but not frank diarrhea or intestinal malabsorption. Vitamin D and beta-carotene levels decreased, but remained within the normal range. In summary, orlistat is the first example of a new class of antiobesity drugs that enhances weight loss and weight maintenance by interfering with dietary fat absorption. Orlistat has tolerable gastrointestinal side effects and no major drug toxicity. Orlistat is a viable adjunct to lifestyle interventions used in the long-term management of obesity.
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PMID:Orlistat for the long-term treatment of obesity. 1297 16

Vitamin D3 is synthesized in the skin during summer under the influence of ultraviolet light of the sun, or it is obtained from food, especially fatty fish. After hydroxylation in the liver into 25-hydroxyvitamin D (25(OH)D) and kidney into 1,25-dihydroxyvitamin D (1,25(OH)2D), the active metabolite can enter the cell, bind to the vitamin D-receptor and subsequently to a responsive gene such as that of calcium binding protein. After transcription and translation the protein is formed, e.g. osteocalcin or calcium binding protein. The calcium binding protein mediates calcium absorption from the gut. The production of 1,25(OH)2D is stimulated by parathyroid hormone (PTH) and decreased by calcium. Risk factors for vitamin D deficiency are premature birth, skin pigmentation, low sunshine exposure, obesity, malabsorption and advanced age. Risk groups are immigrants and the elderly. Vitamin D status is dependent upon sunshine exposure but within Europe, serum 25(OH)D levels are higher in Northern than in Southern European countries. Severe vitamin D deficiency causes rickets or osteomalacia, where the new bone, the osteoid, is not mineralized. Less severe vitamin D deficiency causes an increase of serum PTH leading to bone resorption, osteoporosis and fractures. A negative relationship exists between serum 25(OH)D and serum PTH. The threshold of serum 25(OH)D, where serum PTH starts to rise is about 75nmol/l according to most surveys. Vitamin D supplementation to vitamin D-deficient elderly suppresses serum PTH, increases bone mineral density and may decrease fracture incidence especially in nursing home residents. The effects of 1,25(OH)2D and the vitamin D receptor have been investigated in patients with genetic defects of vitamin D metabolism and in knock-out mouse models. These experiments have demonstrated that for active calcium absorption, longitudinal bone growth and the activity of osteoblasts and osteoclasts both 1,25(OH)2D and the vitamin D receptor are essential. On the other side, bone mineralization can occur by high ambient calcium concentration, so by high doses of oral calcium or calcium infusion. The active metabolite 1,25(OH)2D has its effects through the vitamin D receptor leading to gene expression, e.g. the calcium binding protein or osteocalcin or through a plasma membrane receptor and second messengers such as cyclic AMP. The latter responses are very rapid and include the effects on the pancreas, vascular smooth muscle and monocytes. Muscle cells contain vitamin D receptor and several studies have demonstrated that serum 25(OH)D is related to physical performance. The active metabolite 1,25(OH)2D has an antiproliferative effect and downregulates inflammatory markers. Extrarenal synthesis of 1,25(OH)2D occurs under the influence of cytokines and is important for the paracrine regulation of cell differentiation and function. This may explain that vitamin D deficiency can play a role in the pathogenesis of auto-immune diseases such as multiple sclerosis and diabetes type 1, and cancer. In conclusion, the active metabolite 1,25(OH)2D has pleiotropic effects through the vitamin D receptor and vitamin D responsive elements of many genes and on the other side rapid non-genomic effects through a membrane receptor and second messengers. Active calcium absorption from the gut depends on adequate formation of 1,25(OH)2D and an intact vitamin D receptor. Bone mineralization mainly depends on ambient calcium concentration. Vitamin D metabolites may play a role in the prevention of auto-immune disease and cancer.
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PMID:Vitamin D physiology. 1656 71

Toddlers make a transition from dependent milk-fed infancy to independent feeding and a typical omnivorous diet. This stage is an important time for physicians to monitor growth using growth charts and body mass index and to make recommendations for healthy eating. Fat and cholesterol restriction should be avoided in children younger than two years. After two years of age, fat should account for 30 percent of total daily calories, with an emphasis on polyunsaturated fats. Toddlers should consume milk or other dairy products two or three times daily, and sweetened beverages should be limited to 4 to 6 ounces of 100 percent juice daily. Vitamin D, calcium, and iron should be supplemented in select toddlers, but the routine use of multivitamins is unnecessary. Food from two of the four food groups should be offered for snacks, and meals should be made up of three of the four groups. Parental modeling is important in developing good dietary habits. No evidence exists that early childhood obesity leads to adult obesity, but physicians should monitor body mass index and make recommendations for healthy eating. The fear of obesity must be carefully balanced with the potential for undernutrition in toddlers.
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PMID:Nutrition in toddlers. 1791 Feb 88

Insulin resistance (IR) and central obesity are common features of the polycystic ovary syndrome (PCOS). Vitamin D is thought to play a role in the pathogenesis of type 2 diabetes by affecting insulin metabolism. The aim of our study was to investigate the effect of 25-hydroxyvitamin D (25-OH-VD) on metabolic parameters and IR in PCOS. In 120 untreated PCOS patients (median age 28 years) levels of 25-OH-VD (radioimmunoassay method provided by DiaSorin), calcium and anorganic phosphate were measured. In addition, endocrine and metabolic variables were evaluated and a glucose tolerance test was performed to assess indices of IR. In the entire PCOS cohort, 25-OH-VD concentrations were negatively correlated with body mass index (r=-0.2765), body fat (r=-0.2490), HOMA-IR (r=-0.1947), hyperinsulinemia (r=-0.1892) and leptin levels (r=-0.2834), and positively correlated with HDL cholesterol (r=0.2630) (all p<0.05). Subgroup analysis of lean, overweight and obese women revealed significant higher 25-OH-VD levels in lean women. Differences remained significant when women were divided according to their 25-OH-VD levels. Women with hypovitaminosis D (<9 ng/ml) had higher mean BMI, indices of IR and leptin levels compared to women with normal serum levels (all p<0.05). Analysis of vitamin D and biochemical endocrine PCOS features revealed a significant correlation only between 25-OH-VD and sex hormone-binding globulin as well as the free androgen index. In conclusion, in PCOS women, low 25-OH-VD levels are associated with obesity and insulin resistance but not with PCOS per se.
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PMID:Low serum 25-hydroxyvitamin D concentrations are associated with insulin resistance and obesity in women with polycystic ovary syndrome. 1717 40

In the 1960s, the prevalence of asthma and allergic diseases began to increase worldwide. Currently, the burden of the disease is more than 300 million people affected. We hypothesize that as populations grow more prosperous, more time is spent indoors, and there is less exposure to sunlight, leading to decreased cutaneous vitamin D production. Coupled with inadequate intake from foods and supplements, this then leads to vitamin D deficiency, particularly in pregnant women, resulting in more asthma and allergy in their offspring. Vitamin D has been linked to immune system and lung development in utero, and our epidemiologic studies show that higher vitamin D intake by pregnant mothers reduces asthma risk by as much as 40% in children 3 to 5 years old. Vitamin D deficiency has been associated with obesity, African American race (particularly in urban, inner-city settings), and recent immigrants to westernized countries, thus reflecting the epidemiologic patterns observed in the asthma epidemic. Providing adequate vitamin D supplementation in pregnancy may lead to significant decreases in asthma incidence in young children.
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PMID:Is vitamin D deficiency to blame for the asthma epidemic? 1832 98

Obesity is a risk factor for vitamin D deficiency, but this relation has not been studied among pregnant women, who must sustain their own vitamin D stores as well as those of their fetuses. Our objective was to assess the effect of prepregnancy BMI on maternal and newborn 25-hydroxyvitamin D [25(OH)D] concentrations. Serum 25(OH)D was measured at 4-21 wk gestation and predelivery in 200 white and 200 black pregnant women and in their neonates' cord blood. We used multivariable logistic regression models to assess the independent association between BMI and the odds of vitamin D deficiency [25(OH)D <50 nmol/L] after adjustment for race/ethnicity, season, gestational age, multivitamin use, physical activity, and maternal age. Compared with lean women (BMI <25), pregravid obese women (BMI >or=30) had lower adjusted mean serum 25(OH)D concentrations at 4-22 wk (56.5 vs. 62.7 nmol/L; P < 0.05) and a higher prevalence vitamin D deficiency (61 vs. 36%; P < 0.01). Vitamin D status of neonates born to obese mothers was poorer than neonates of lean mothers (adjusted mean, 50.1 vs. 56.3 nmol/L; P < 0.05). There was a dose-response trend between prepregnancy BMI and vitamin D deficiency. An increase in BMI from 22 to 34 was associated with 2-fold (95% CI: 1.2, 3.6) and 2.1-fold (1.2, 3.8) increases in the odds of mid-pregnancy and neonatal vitamin D deficiency, respectively. The rise in maternal obesity highlights that maternal and newborn vitamin D deficiency will continue to be a serious public health problem until steps are taken to identify and treat low 25(OH)D.
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PMID:Prepregnancy obesity predicts poor vitamin D status in mothers and their neonates. 1795 82


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