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

We studied the occurrence of osteopenia, as reflected by decreased cortical bone thickness, in a nonobese animal model of hereditary non-insulin-dependent diabetes with long duration, i.e., 8-month-old Goto-Kakizaki (GK) rats. In addition, motor nerve-conduction velocity was measured in the GK rats. Age- and weight-matched Wistar rats served as controls. The GK rats displayed marked glucose intolerance, as compared to control rats, in an intraperitoneal glucose tolerance test. Decreased cortical bone thickness by approximately 15%, was evident in X-ray analysis of metatarsal bones (p < 0.001) and humerus (p < 0.05) of the GK rats. Motor nerve-conduction velocity, measured in the sciatic nerve, was also decreased (by 10%) in the GK as compared with the age-matched control rats (p < 0.05). In conclusion, reduction of cortical bone thickness is present in 8-month-old GK rats, which simultaneously demonstrate signs of peripheral neuropathy. Thus, the GK rat appears to be a model of NIDDM suitable for studies of diabetic bone disease in the absence of obesity.
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PMID:Decreased cortical bone thickness in spontaneously non-insulin-dependent diabetic GK rats. 936 71

African teenagers with slipped capital femoral epiphysis (SCFE) not infrequently also have genu valgum (knock-knee). Because we had previously demonstrated metabolic bone disease attributable to dietary calcium deficiency in black teenagers with genu valgum, we examined 29 black teenagers (15 male, 14 female) with SCFE for metabolic bone disease. Each patient had an iliac crest bone biopsy taken (after double tetracycline labeling) for routine histomorphometry, and blood and urine samples for bone biochemistry. Spinal bone mineral density was measured in 13 patients. Compared to reported data, we found our patients to be sexually more immature, older, at least as obese, and to have more severe and more frequently bilateral hip disease. Eighty percent of the children took dairy products only once or twice a week or less frequently, and 37.9% had genu valgum. Compared with race- and age-matched South Africans, bone biopsies in our patients showed lower bone volume (BV/TV, p = 0.0003), wall thickness (p = 0.0002), and trabecular thickness (Tb.Th, p = 0.0002), and a tendency to greater trabecular spacing (Tb.Sp, p = 0.053). Lower osteoid volume (OV/BV, p = 0.0001), osteoid surface (OS/BS, p = 0.0001), osteoid thickness (O.Th, p = 0.0002), double labeled surface (dLS/BS, p = 0.029), and bone formation rate (BFR/BS, p = 0.037) suggested poorer bone forming capacity in our patients. No evidence of hyperparathyroid bone disease or osteomalacia was found. BV/TV was below the reference range (14.2%) in 65.5% of cases; these patients had lower values for Tb.Th (p = 0.037) and Tb.N (p = 0.0003), greater Tb.Sp (p = 0.0002), a tendency to lower adjusted apposition rate (Aj.AR, p = 0.057), and had had less frequent intake of dairy products than those with normal BV/TV (p = 0.024). Furthermore, months since menarche correlated with histomorphometric variables BV/TV (r = 0.667, p = 0.009), Tb.Th (r = 0.745, p = 0.002), Tb.Sp (r = -0.549, p = 0.042), O.Th (r = 0.784, p = 0.0009), and Aj.AR (r = 0.549, p = 0.042). The correlation between Tb.Th and spinal bone mineral content (r = 0.656, p = 0.015) suggests that the reduced trabecular thickness reflected a generalized bone condition. A greater than normal proportion of patients had spinal bone mineral density values below -1 standard deviation (SD) of the mean (osteopenia) (p = 0.001). Patients tested for parathyroid hormone and 25-hydroxyvitamin D levels were found to have normal values. Parathyroid hormone correlated with Aj.AR (r = 0.661, p = 0.038) and serum phosphorus (r = -0.764, p = 0.010). We conclude that sexual immaturity and possibly past dietary calcium deficiency contributed to osteopenia, and that this, together with obesity, led to the development of more severe and more frequently bilateral SCFE in our patients than in reported series of black and white children.
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PMID:Bone disease in African children with slipped capital femoral epiphysis: histomorphometry of iliac crest biopsies. 951 18

Liver transplantation is now routinely used as a definitive treatment for patients with advanced cirrhosis. As survival after transplantation in most centers is at or above 70% to 80% at 1 year, an increasing number of liver transplant recipients requires further medical care. Several medical complications may develop during the immediate or long-term postoperative periods, including renal dysfunction, arterial hypertension, neurological complications, and psychiatric complications. In addition, other metabolic complications often develop in a more insidious manner, such as obesity, hyperlipidemia, diabetes mellitus, and posttransplant bone disease. Because the liver allograft function is frequently normal in many recipients experiencing the above-mentioned complications, the gastroenterologist, internist, or family practitioner frequently has a role in the diagnosis and management of these complications. In this review, we discuss the basic pathophysiological concepts and suggest guidelines for the diagnosis and management of frequent medical problems encountered after liver transplantation.
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PMID:Common medical diseases after liver transplantation. 970 Aug 42

The aim of this study was to determine the efficacy and safety of two malabsorptive procedures for severe obesity. Prospectively collected data from eight men and three women who underwent partial biliopancreatic bypass (PBB) and 19 men and seven women who underwent very very long limb Roux-en-Y gastric bypass (VVLGB) for superobesity (preoperative weight >225% above ideal body weight) were evaluated. Age (42 +/- 3 years and 40 +/- 2 years), body mass index (64 +/- 4 kg/m(2) and 67 +/- 3 kg/m(2)), and percentage of excess body weight (183% +/- 17% and 203% +/- 12%) were similar (mean +/- standard error of the mean). Median follow-up was 96 months (range 72 to 108 months) and 24 months (range 18 to 60 months) for the PBB and VVLGB groups, respectively. Weight loss expressed as percentage of excess body weight was 68% +/- 4% 2 years and 71% +/- 5% 4 years after PBB, and 53% +/- 7% 2 years and 57% +/- 5% 4 years after VVLGB. Current body mass indexes are 37 +/- 2 kg/m(2) and 42 +/- 2 kg/m(2) in the PBB and VVLGB groups, respectively. Hospital mortality was zero. Morbidity occurred in five patients after VVLGB (wound infection in four, wound seroma in one, and pulmonary embolus in one) and in two patients after PBB (abscess in two, anastomotic leak in one, and gastrointestinal bleeding in one). After PBB, one woman died of refractory liver failure 18 months postoperatively and two other patients developed metabolic bone disease. No such known complications have occurred to date after VVLGB. We conclude that VVLGB is safe and effective for clinically significant obesity, results in sustained weight loss, and improves quality of life.
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PMID:Malabsorptive procedures for severe obesity: comparison of pancreaticobiliary bypass and very very long limb Roux-en-Y gastric bypass. 1055 67

Many liver transplant recipients are now reaching survival beyond 5 years from the liver transplant procedure, and many others are alive more than a decade from acquiring their new liver. Orthotopic liver transplant recipients enjoy the benefits of normal liver function, but a variety of metabolic and other medical problems often develop that require diagnosis and adequate management. These problems include hyperlipidemia, obesity, diabetes mellitus, renal disfunction, arterial hypertension, bone disease and neuropsychiatric syndromes. The gastroenterologist, internist, or local family physician is frequently called on to identify and treat these postoperative complications in conjunction with physicians at the transplant center.
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PMID:Long-term care of the liver transplant recipient. 1123 68

1. Forty percent of transplant centers expect the primary care physician to be the primary physician; 40% have both a primary care physician and a hepatologist manage the patient. 2. Transplant centers expect primary care physicians to provide general preventive medicine, physical examinations, vaccinations, and, rarely, management of hypertension, renal dysfunction, and diabetes. 3. A high percentage of primary care physicians feel comfortable caring and managing the overall health care of a long-term liver transplant patient. 4. Primary care physicians feel at most ease managing preventive care, annual physical examinations, hypertension, diabetes mellitus, hyperlipidemia, bone disease, and vaccinations. 5. Primary care physicians should be aware of the common medical conditions of the liver transplant patient of hypertension, diabetes, obesity, hyperlipidemia, and recurrent disease. 6. Common medical conditions for both the transplant centers and primary care physicians are hypertension, dyslipidemia, diabetes mellitus, malignancy, bone disease, pregnancy, vaccination, infectious prophylaxis, and headaches.
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PMID:Posttransplantation care: role of the primary care physician versus transplant center. 1168 71

Chronic kidney disease (CKD) is a permanent, progressive loss of kidney function characterized by a decline in glomerular filtration rate (GFR). Early identification of CKD risk factors provides an opportunity to prevent or delay the progression of kidney disease and decrease morbidity and mortality. There is increasing evidence to suggest that the adverse outcomes of CKD can be delayed or prevented by early detection and treatment. Current literature suggests that a low-protein, low-phosphorus diet may retard the progression of kidney disease. Other modifiable risk factors affecting CKD include proteinuria, hypertension, hyperglycemia, dyslipidemia, bone disease, anemia, and obesity. This discussion will review the current clinical nutrition guidelines for managing adult patients with CKD.
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PMID:Integrating clinical nutrition practice guidelines in chronic kidney disease. 1620 58

We have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreases the serum phosphate. Most recently, these observations were rediscovered in low-density lipoprotein receptor null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance). We had demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial type. We have shown that VC is worsened by CKD and ameliorated by bone morphogenetic protein -7 (BMP-7). The finding that high-fat-fed low-density lipoprotein receptor null animals without CKD have hyperphosphatemia led us to examine the skeletons of these mice. We found significant reductions in bone formation rates, associated with increased VC and superimposing CKD results in the adynamic bone disorder (ABD), while VC was worsened and hyperphosphatemia persisted. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. BMP-7 treatment corrected the ABD and corrected hyperphosphatemia, compatible with BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. Thus, in the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to ABD producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through increased bone formation and skeletal deposition of phosphate, and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury before demonstrable hyperphosphatemia, and they are preventable and treatable. Therefore, early intervention in CKD is warranted and may affect mortality of the disease.
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PMID:Connections between vascular calcification and progression of chronic kidney disease: therapeutic alternatives. 1633 68

Patients with chronic kidney disease (CKD) have high rates of healthcare utilization, morbidity, and mortality. Increasing rates of obesity, diabetes, and hypertension suggest that the expected numbers of patients with CKD will rise. Managing the economic and clinical burden of CKD will be a significant challenge for the healthcare system. The burden of CKD can be considered in terms of both CKD-specific and CKD-related morbidity and mortality. CKD-specific complications include anemia and bone disease. CKD-related complications include obesity, diabetes and hypertension. CKD-specific complications tend to occur later in the course of disease and may be best treated by a nephrologist, while CKD-related complications may be most easily treated by primary care physicians. Coordinating patient care is essential to managing the burden of this growing disease.
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PMID:Managing the burden of chronic kidney disease. 1662 Jan 97

Vitamin D deficiency is common in Arab countries particularly among women. This is the result of a low dietary intake of the vitamin, limited exposure to sunlight (a paradox in view of the high sunshine figures), skin colour, obesity and high parity. Apart from its adverse effects on bone in women and their offspring, vitamin D deficiency has the potential to cause or exacerbate heart failure through a number of mechanisms including activation of the renin-angiotensin system and increased arterial pressure. Accordingly, we propose that ensuring adequate vitamin D levels in Arab women will have a much greater impact on health than just the prevention of bone disease. In particular, we suggest that prevention and correction of vitamin D deficiency will reduce the incidence of heart failure and, for Arab women with established heart failure and vitamin D deficiency, improve cardiac function.
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PMID:Hypothesis: Correction of low vitamin D status among Arab women will prevent heart failure and improve cardiac function in established heart failure. 1682 39


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