Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal osteodystrophy in hemodialyzed patients with DM-HD shows different features from that in non-DM,HD. Two studies were done. One was a comparison of BMD in 30 non-DM,HD patients and 30 DM-HD patients. The second was a comparison of possible factors affecting calcium metabolism in the higher and lower BMD groups (n = 20/21) in the DM-HD patients. BMD was measured by dual-energy X-ray absorptiometry (DEXA; Hologic QDR 1,000/W) in the third lumbar vertebra (L3), head, pelvis, and whole body. The BMDs of the DM-HD group were lower in these areas and whole body than that in the non-DM,HD group. A significant difference was found in the head BMD (p less than 0.05). In the second study, factors which may contribute to the differences in BMD were compared in the DM-HD patients divided into higher and lower BMD of the head. The group with higher head BMD had a value 110% of the mean value or more. Clinical and biochemical test results (age, the time since the first dialysis, body weight, the degree of obesity, height, serum calcium, serum phosphate, serum aluminum, serum c-PTH level and the dose of 1 alpha-OH-D3) were compared. The degree of obesity of the patients with higher BMD was significantly larger than that with lower BMD (p less than 0.005).
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PMID:Decreased bone mineral density in diabetic patients on hemodialysis. 195 51

BMC and BMD of the total body bone and lumbar spine were measured in normal control and patients with metabolic bone diseases by DPA (Dichromatic Bone Densitometer Model 2600, Norland corporation). Also, total body fat mass was measured in patients with obesity. We discussed basic technical problems and showed some data to assess patients with metabolic diseases known to affect the skeleton such as primary and secondary hyperparathyroidism. DPA is useful technique to assess patients with metabolic bone diseases and to monitor the efficacy of treatments.
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PMID:[Dual photon absorptiometry]. 231 20

This study was undertaken to evaluate the effect of obesity on the postmenopausal bone mass. Bone mineral density, measured by dual photon absorptiometry of the lumbar spine, serum osteocalcin (OC), fasting urinary calcium to creatinine (Ca:Cr), serum estradiol (E2) dehydroepiandrosterone (DHA) and testosterone (T) were measured in 176 women aged 45-71 years. Women were divided into four groups according to their menopausal status and their weight: 49 perimenopausal, 28 obese perimenopausal, 49 obese postmenopausal. Within each population (perimenopausal and postmenopausal), mean age was the same, only weight was significantly different (p less than 0.0001). For the two groups of postmenopausal women mean interval since menopause (YSM) was the same (5.8 +/- 3 and 5.4 +/- 5 yr). Comparison between groups revealed a significant effect of menopausal status and obesity on BMD and bone turnover. As compared to perimenopausal women, BMD was lower, OC and Ca: Cr higher only in nonobese-postmenopausal women. E2, T, DHA did not differ between the two groups of postmenopausal women. The results of this study suggest that even moderate obesity can play a protective role on postmenopausal bone loss.
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PMID:Obesity and postmenopausal bone loss: the influence of obesity on vertebral density and bone turnover in postmenopausal women. 296 34

The association of OA with increased bone mass is controversial. This study measured BMD at the hip and spine and total body bone mineral (TBBM) by dual energy X-ray absorptiometry, and BMD at the distal forearm by single photon absorptiometry in 20 post-menopausal women with primary generalized OA. The data were compared with those from 89 normal controls. Osteoarthritic women had significantly increased BMD at the spine (P < 0.001), distal forearm (P < 0.05) and increased TBBM (P < 0.01), but no difference was seen at the femoral neck. These differences were not explained by obesity. The influence of mobility is discussed.
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PMID:Primary generalized osteoarthritis and bone mass. 825 14

In order to test the impact of a given risk profile on the incidence of osteoporosis which could justify BMD measurement, and that of a low risk profile which could render it unnecessary, BMD was measured in 217 women under 72 in whom menopause had occurred at least 6 years previously and who corresponded to one of the two following profiles: high risk (A, n = 102) = BMI < 27 kg/m2, with no estrogen replacement treatment, and with at least one of the following risk factors: BMI < 20, early menopause, positive family history, no dairy products associated with tobacco consumption (> 10 cigarettes/day for > 20 years and/or alcohol consumption of > 0.5 l wine/day during > 10 years, corticotherapy of > 6 months, rickets, anorexia nervosa. Low risk (B, n = 115) = absence of characteristics of group A, BMI > 27 kg/m2 with (B+, n = 24) or without estrogen therapy (B-, n = 91). BMD was measured by DXA in 4 centers using Lunar or Hologic equipment. Results were expressed in % of the mean of the respective young adult control groups. As expected, BMD was significantly different in these two subgroups of the population. Osteoporosis was diagnosed (BMD < 75% = < -2.5 SD, according to WHO) in 72% of group A, and in 17% (B+) and 19% (B-) respectively of group B. There was no difference between the various risk factors in group A concerning their impact on BMD, but concerning incidence, low BMI and early menopause were the most frequent. The high risk profile of group A seems to justify densitometry, since it leads to the diagnosis of osteoporosis in over 70%. However, the protective profile of group B does not exclude osteoporosis (risk still 20%); only in severe obesity (BMI > 33) does it drop to 1%.
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PMID:[Importance of the clinical profile in the postmenopausal osteoporosis screening by densitometry]. 876 76

The effect of weight, classified by body mass index (BMI), on bone mass (BMC) of the whole body and on bone mineral density BMD of the hip joint was analysed in a sample of 120 Austrians of Vienna and surroundings. The 68 females and 52 males of this cross sectional study ranged in age between 60 and 92 years (x = 71.7 +/- 7.7). Age distribution was not significantly different between sexes. The WHO (1997) classification of body mass index (BMI) was used for weight classification, i.e. normal weight (BMI 18.5-24.99) and moderate overweight (BMI 25.0-29.99). Obese subjects (BMI 30+) were not included in this study. Bone mass of the whole body as well as bone density of the hip joint were determined by Dual-energy-X-ray absorptiometry (DEXA) using a hologic 2000 scanner. As expected BMC and BMD values were significantly higher in males than in females. While in both females and males moderately overweight BMD of the hip was significantly higher than in those with normal BMI, statistically significant differences of BMC were restricted to females only. Such positive association between body weight and BMC and BMD is in agreement with previous studies on mature subjects, and menopausal and postmenopausal women in particular. In addition, this study demonstrates corresponding positive associations between moderate overweight and bone mass and -density in the elderly and old aged.
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PMID:Protective effect of moderate overweight on bone density of the hip joint in elderly and old Austrians. 1216 64

Uncouplers of oxidative phosphorylation have relevance to bioenergetics and obesity. The mechanisms of action of chemical uncouplers of oxidative phosphorylation on biological systems were evaluated using differential gene expression. The transcriptional response in human rhabdomyosarcoma cell line (RD), was elucidated following treatment with carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), a classical uncoupling agent. Changes in mitochondrial membrane potential were used as the biological dosimeter. There was an increase in membrane depolarization with increasing concentrations of FCCP. The concentration at 75% uncoupling (20 microM) was chosen to study gene expression changes, using cDNA-based large-scale differential gene expression (LSDGE) platforms. At the above concentration, subtle light microscopic and clear gene expression changes were observed at 1, 2, and 10 h. Statistically significant transcriptional changes were largely associated with protein synthesis, cell cycle regulation, cytoskeletal proteins, energy metabolism, apoptosis, and inflammatory mediators. Bromodeoxyuridine (BrdU) and propidium iodide (PI) assays revealed cell cycle arrest to occur in the G1 and S phases. There was a significant initial decrease in the intracellular adenosine triphosphate (ATP) concentrations. The following seven genes were selected as potential molecular markers for chemical uncouplers: seryl-tRNA synthetase (Ser-tRS), glutamine-hydrolyzing asparagine synthetase (Glut-HAS), mitochondrial bifunctional methylenetetrahydrofolate dehydrogenase (Mit BMD), mitochondrial heat shock 10-kDa protein (Mit HSP 10), proliferating cyclic nuclear antigen (PCNA), cytoplasmic beta-actin (Act B), and growth arrest and DNA damage-inducible protein 153 (GADD153). Transcriptional changes of all seven genes were later confirmed with reverse transcription-polymerase chain reaction (RT-PCR). These results suggest that gene expression changes may provide a sensitive indicator of uncoupling in response to chemical exposure.
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PMID:Effects of minimally toxic levels of carbonyl cyanide P-(trifluoromethoxy) phenylhydrazone (FCCP), elucidated through differential gene expression with biochemical and morphological correlations. 1270 Apr

The purpose of this study was to determine the relationship between BMD and childhood obesity. We examined 1070 obese children (722 boys and 348 girls) aged 7 to 15 years. Their mean relative weight, as a percentage of the standard weight for age, height, and sex, was 152.9 +/- 14%. BMD was assessed, by a digital image processing method, in the second metacarpal bone of the left hand. We compared our results with those of healthy nonobese Japanese children based on both chronological and bone age. Mean BMD values for bone age in the obese children were significantly higher than those in control groups in boys aged 11 years and under and girls 9 years and under. On the other hand, in boys over 12 years old, BMD values for bone age were lower than those in the control groups. In girls over 11 years old, BMD values tended to be lower than those in the control groups. In conclusion, we studied the BMD of obese children from the point of view of advanced bone age. Our results showed that BMD was higher than in prepubertal obese children, but a low BMD value was found after puberty, due to poor gain of BMD during puberty. It is important to prevent obesity in childhood in order to prevent the low BMD after puberty.
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PMID:Obese Japanese children have low bone mineral density after puberty. 1522 98

Leptin is a hormone involved with satiety and energy balance and proposed to be an anti-obesity factor. Much effort has been dedicated to the relationship between leptin and bone. This interest stems from the knowledge that body weight is a major determinant of bone density. It is known that obese persons have stronger bones and lose bone tissue at a slower pace. Therefore, attention has been given to leptin as a mediator of increased osteogenesis. Leptin has been shown to play a role on bone both in vitro and in vivo. The administration of leptin in vitro induced the expression of leptin receptors on stromal cells, the differentiation to osteoblasts and inhibition of differentiation into the adipocyte phenotype. In addition, leptin was able to inhibit osteoclastogenesis of peripheral blood mononuclear cells. Therefore, there is in vitro and experimental evidence that leptin is able both to stimulate osteoblasts and inhibit osteoclast differentiation. This would be in line with the hypothesis that the correlation between obesity and increased BMD is linked to leptin activity. However, experimental results are indicative of a role of CNS in mediating the effect of leptin on bone metabolism. These effects are opposite to the direct effects on bone cells and lead to bone loss. To solve the problem, it has been suggested that obese individuals have a resistance of nervous structures to leptin. In chronic renal failure serum leptin levels are markedly increased. An inverse correlation between histomorphometric parameters of bone turnover and serum leptin levels and between leptin and PTH have been reported. Therefore, the hypothesis has been raised that leptin lowers bone turnover in chronic renal failure. Since leptin has a direct stimulatory effect on bone and an indirect opposite effect via the CNS, it has been suggested that in CRF a resistance of nervous structures to leptin, like in obesity, may be present. By now, coherent findings suggest that the prevailing effect of leptin on bone in ESRD is that of reducing bone turnover.
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PMID:Leptin and bone metabolism. 1529 17

Childhood obesity is prevalent and linked to the development of Type 2 diabetes mellitus (DM) and poor bone health. Some PUFA enhance bone mass and thus may improve bone health in obese children. The study objective was to determine the effects of dietary (n-6) compared with (n-3) essential PUFA and long-chain PUFA (LCPUFA) on bone in an obese and insulin-resistant state. Male fa/fa (n = 48) and lean Zucker rats (n = 48) were fed diets containing safflower oil [SO, high (n-6) PUFA], flaxseed oil [FXO, high (n-3) PUFA], or menhaden oil [MO, high (n-3) LCPUFA] for 9 wk. Measurements included the following: femur bone area (BA), mineral content (BMC), density (BMD), morphometry and ex vivo release of prostaglandin E(2) (PGE(2)); plasma osteocalcin and C-terminal telopeptides of type I collagen. Differences among groups were detected using 2-way ANOVA. Genotype effects in the fa/fa rats included lower femoral weight, length, BA, and BMC, as well as femoral head and proximal epiphysis widths compared with the lean rats, but BMD was not affected. Femur BA, BMC, and BMD did not differ among the dietary groups, but diaphysis width was elevated in the MO group and PGE(2) release was reduced by the FXO and MO diets. No genotype x diet interactions were observed. These data indicate that the fa/fa Zucker rat is at risk for low bone mass and that dietary (n-3) FA effectively reduce PGE(2) release. Whether reduced PGE(2) will support optimal peak bone mass during childhood and conserve bone mass with aging warrants investigation.
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PMID:(n-3) fatty acids reduce the release of prostaglandin E2 from bone but do not affect bone mass in obese (fa/fa) and lean Zucker rats. 1573 84


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