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 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Successful kidney transplantation leads to restoration of renal function. Some metabolic disorders from chronic renal failure may persist and new metabolic abnormalities can develop (obesity, diabetes, hypertension, bone disease, and anemia). Additionally, influence of immunosuppressive drugs (corticosteroids, cyclosporine A, tacrolimus, and rapamycin) may aggravate the course of diabetes, hypertension, and dyslipidemia. Nutritional management of renal transplantation is divided into the pretransplant period, transplant surgery, and early and late posttransplant period. Patients in the pretransplant period in dialysis treatment may develop protein-energy malnutrition and negative nitrogen balance, with loss of lean body mass and fat deposits. Nutritional management in the early posttransplant period with a functioning kidney graft necessitates fluid and electrolyte balance control with protein intake of 1,2/kg BW/day and 30-35 kcal/kg BW/day. In a nonfunctioning kidney graft, dialysis treatment continues and the therapeutic dose of immunosuppressive drugs must be reduced. The principal objective in the late posttransplant period is the maintenance of optimal nutritional status. Nutrition is important in managing obesity, insulin resistance, diabetes, hyperlipidemia, and hypertension. Other posttransplant conditions for which diet and/or nutritional supplements may be beneficial include hypomagnesemia, hypophosphatemia, hyperuricemia, hyperkalemia, hyperhomocysteinemia, chronic renal allograft failure, renal anemia, and renal bone disease.
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PMID:Nutritional consequences of renal transplantation. 1912 81

Epidemiological studies suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in human offspring. Animal models provide a means of assessing the independent consequences of altering the pre- vs postnatal environments on a variety of metabolic, physiological and neuroendocrine functions, which lead to the development of offspring obesity, diabetes, hypertension and hyperlipidemia. During the gestational period, maternal malnutrition, obesity, type 1 and type 2 diabetes, and psychological and pharmacological stressors can all promote offspring obesity. Normal postnatal nutrition can sometimes reduce the adverse effect of some of these prenatal factors, but may also exacerbate the development of obesity and diabetes in offspring of dams that are malnourished during gestation. The genetic background of the individual is also an important determinant of outcome when the perinatal environment is perturbed. Individuals with an obesity-prone genotype are more likely to be adversely affected by factors such as maternal obesity and high-fat diets. Many perinatal manipulations are associated with reorganization of the central neural pathways which regulate food intake, energy expenditure and storage in ways that enhance the development of obesity and diabetes in offspring. Both leptin and insulin have strong neurotrophic properties so that an excess or an absence of either of them during the perinatal period may underlie some of these adverse developmental changes. As perinatal manipulations can permanently and adversely alter the systems that regulate energy homeostasis, it behooves us to gain a better understanding of the factors during this period that promote the development of offspring obesity as a means of stemming the tide of the emerging worldwide obesity epidemic.
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PMID:Synergy of nature and nurture in the development of childhood obesity. 1936 9

In nonalcoholic fatty liver disease, oxidative stress is believed to play a crucial role as a second-hit for the progression of simple steatosis to steatohepatitis. Thioredoxin (TRX) is a potent antioxidant molecule that exerts anti-apoptotic and anti-inflammatory functions. TRX-binding protein-2 (TBP-2) is an endogenous negative regulator of TRX. Deficiency of TBP-2 in mice causes hyperlipidemia, hepatic steatosis, hypoglycemia, and bleeding tendency, resembling Reye syndrome in a fasting/glucose-deficient state. The aim of this study was to investigate the role of TBP-2 in the development of nonalcoholic steatohepatitis (NASH). TBP-2-deficient (TBP-2(-/-)) and wild-type (WT) mice were fed either a normal or methionine-choline-deficient (MCD) diet for up to 10 weeks. Compared with WT mice, TBP-2(-/-) mice showed severe simple steatosis rather than steatohepatitis. However, oxidative stress determined by lipid peroxidation and DNA damage, neutrophil infiltration, and hepatic fibrosis were attenuated in TBP-2(-/-) mice. PCR analysis showed the expressions of fibrosis-inducing and inflammatory cytokine-related genes were less in TBP-2(-/-) mice. Moreover, leptin, SREBP1c, PPARgamma, and adipogenesis-lipogenesis-related genes were upregulated in TBP-2(-/-) mice. These results strongly suggested that TBP-2 might be involved in pathogenesis of NASH in WT mice, and inhibitors of TBP-2 could be useful in the prevention or treatment of NASH.
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PMID:Thioredoxin-binding protein-2 deficiency enhances methionine-choline deficient diet-induced hepatic steatosis but inhibits steatohepatitis in mice. 1976 81

Deficiency of adiponectin (APN), an adipocyte-derived vascular protective molecule, contributes to diabetic vascular injury. The current study determined whether obesity/hyperlipidemia may alter the vascular response to APN, and investigated the involved mechanisms and pathologic significance. Adult male Sprague-Dawley rats were fed a regular or high-fat diet (HF) for 4-16 weeks. Circulating APN levels, aortic pAMPK/AMPK, peNOS/eNOS, and APN receptor expression levels were determined. Compared to time-matched animals fed control diet, plasma APN levels in HF-diet animals were significantly increased at 8 weeks, and rapidly declined thereafter. Despite unchanged or elevated circulating APN levels, phosphorylated AMPK and eNOS in vascular tissue were significantly reduced at all observed time points. Recombinant full-length APN (rAPN)-induced AMPK/eNOS phosphorylation and vasodilatation were significantly reduced in 16-week obese/hyperlipidemic aortic segments. Vascular APN receptor 1 (AdipoR1) and receptor 2 (AdipoR2) expression were significantly reduced 16 weeks after HF-diet. Pre-incubation of rAPN with obese/hyperlipidemic plasma, but not with normal plasma, significantly reduced its AMPK and eNOS activation effect, and blunted its protective effect against TNFalpha-induced HUVEC apoptosis. This study demonstrated for the first time that obesity/hyperlipidemia reduces vascular responsiveness to APN. Modification/inactivation of APN by unidentified factors present in obese/hyperlipidemic plasma, decreased vascular AdipoR1/R2 expression, and reduced circulating APN levels contribute to reduced vascular responsiveness to APN at different stages of the obese condition. Reduced APN bioactivity allows unmitigated TNFalpha pro-apoptotic and pro-inflammatory actions, contributing to vascular injury in obesity/hyperlipidemia.
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PMID:Reduced vascular responsiveness to adiponectin in hyperlipidemic rats--mechanisms and significance. 2030 76

Cholesterol 7alpha-hydroxylase (CYP7A1) plays a key role in maintaining lipid and bile salt homeostasis as it is the rate-limiting enzyme converting cholesterol to bile acids. Deficiency of CYP7A1 leads to hyperlipidemia in man and mouse. Hyperlipidemia is often seen in patients when treated with high-dose retinoic acid (RA), but the molecular mechanisms remain elusive. Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Promoter reporter assays demonstrate that all-trans RA (atRA) specifically activated FXR/RXR. However, detailed molecular analyses indicate that this activation is through RXR, whose ligand is 9-cis RA. Knocking down of FXR or RXRalpha by small interference RNA (siRNA) in human hepatocytes increased CYP7A1 basal expression, but the repressive effect of atRA persisted, suggesting there are also FXR/RXR-independent mechanisms mediating atRA repression of CYP7A1 expression. Chromatin immunoprecipitation (ChIP) assay and cell transfection results indicate that PGC-1alpha plays a role in the FXR/RXR-independent mechanism. Our findings may provide a potential explanation for hyperlipidemic side effects observed in some patients treated with high-dose RA.
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PMID:Retinoic acid represses CYP7A1 expression in human hepatocytes and HepG2 cells by FXR/RXR-dependent and independent mechanisms. 2033 15

Homocysteine is an amino acid that appears to damage the vascular endothelium and promote thrombosis. The most frequent causes of hyperhomocyst(e)inemia are the inherited defect of the enzyme cystathinonine B-synthase and nutritional deficiency of vitamin B(12) or folate. Hyperhomocyst(e)inemia is associated, perhaps causally, with atherosclerotic vascular disease. Interactions with risk factors such as cigarette smoking, hyperlipidemia, and hypertension are possible, but not yet defined. Dietary supplementation with vitamin B(12), folate, and other substances can reduce homocysteine levels. Such simple measures may reduce the risk of vascular disease in hyperhomocyst(e)inemic subjects.
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PMID:Homocysteine as a risk factor for cardiovascular disease. 2123 3

Malnutrition and dehydration are common and result from swallowing disorders secondary to degeneration of brainstem motor neurons. Recent knowledge argues in favor of the associated primary metabolism abnormalities. Though muscle atrophy, a paradoxical hypermetabolism at rest has often been observed. Hyperlipidemia and glucose intolerance are more frequent than in general population. The heterogeneity of the nutritional assessment of patients in published series is due, partially at least, to the use of disparate criteria and evaluating procedures. Weight lost is an independent negative survival prognostic factor. Overweight may be beneficial for the survival of ALS patients. A specific nutritional management for ALS is an essential point in the multidisciplinary support. The criteria leading to artificial nutrition indication are medical, mainly based on percentage of weight loss, but also psychological and ethical.
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PMID:[Nutritional management in amyotrophic lateral sclerosis: A medical and ethical stake]. 2213 88

Worldwide, obesity is the most prevalent form of malnutrition. It is one of the most significant contributors to ill health and an indirect cause of morbidity and mortality resulting from hyperlipidaemia and glucose intolerance. Very few studies on the prevalence of obesity have been reported from developing countries like India. The present study was therefore undertaken to determine the prevalence of obesity and its predictors in the Indian community. The objectives are: (1) To determine the prevalence of obesity, (2) to study the relationship of obesity with age, (3) to identify the predictors of obesity. This community-based cross-sectional study was conducted on 801 subjects, aged 20 years and above in Kanpur District, using multistage stratified random sampling technique. Data was analysed using the software statistical package for social sciences 10.0.1 for windows. Prevalence of obesity was found to be 4.7%. An increase in body mass index was seen with increasing age. A higher prevalence of obesity was seen in the urban population and in women. Age, gender and daily intake of saturated fatty acids were found to be the main predictors of the obesity. An increase in the level of physical activity resulted in a decrease in the prevalence of obesity (odd's ratio = 0.36). Obesity is an emerging public health problem in the Indian population which indicates that intervention at the primary healthcare level, especially in diet and activity, are important for its prevention.
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PMID:Prevalence and determinants of obesity in the adult population of Kanpur district -- a population-based study. 2231 58

Chronic kidney disease is becoming a major health problem globally and in India an alarming number of about 8 million people are suffering from this disease. Patients undergoing hemodialysis have a high prevalence of protein-energy malnutrition and inflammation. As these two conditions often occur concomitantly in hemodialysis patients, they have been referred together as 'malnutrition-inflammation-atherosclerosis syndrome' to emphasize the important association with atherosclerotic cardiovascular disease. The three factors related to the pathophysiology in these patients are dialysis related nutrient loss, increased protein catabolism and hypoalbuminemia. Inflammation in Chronic Kidney disease is the most important factor in the genesis of several complications in renal disease. Pro-inflammatory cytokines like IL-1 and TNF-alpha play a major role in the onset of metabolic alterations in Chronic Kidney disease patients. Atherosclerosis is a very frequent complication in uremia due to the coexistence of hypertension, hyperhomocysteinemia, inflammation, malnutrition and increased oxidative stress, generation of advanced glycation end products, advanced oxidation protein products, hyperlipidemia and altered structural and functional ability of HDL. LDL-cholesterol, apolipoprotein (A), apolipoprotein (B), and Lp(a) are also associated with atherosclerosis. Studies have now provided enormous data to enable the evaluation of the severity of malnutrition-inflammation-atherosclerosis syndrome as well as effective monitoring of these patients.
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PMID:Malnutrition-inflammation-atherosclerosis syndrome in Chronic Kidney disease. 2310 56

Regucalcin (RGN/SMP30) was originally discovered in 1978 as a unique calcium-binding protein that does not contain the EF-hand motif of calcium-binding domain. The regucalcin gene (rgn) is localized on the X chromosome and is identified in over 15 species consisting the regucalcin family. Regucalcin has been shown to play a multifunctional role in cell regulation; maintaining of intracellular calcium homeostasis and suppressing of signal transduction, translational protein synthesis, nuclear deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) synthesis, proliferation, and apoptosis in many cell types. Moreover, regucalcin may play a pathophysiological role in metabolic disorder. The expression of regucalcin is stimulated through the action of insulin in liver cells in vitro and in vivo and it is decreased in the liver of rats with type I diabetes induced by streptozotocin administration in vivo. Overexpression of endogenous regucalcin stimulates glucose utilization and lipid production in liver cells with glucose supplementation in vitro. Regucalcin reveals insulin resistance in liver cells. Deficiency of regucalcin induces an impairment of glucose tolerance and lipid accumulation in the liver of mice in vivo. Overexpression of endogenous regucalcin has been shown to decrease triglyceride, total cholesterol and glycogen contents in the liver of rats, inducing hyperlipidemia. Leptin and adiponectin mRNA expressions in the liver tissues are decreased in regucalcin transgenic rats. Decrease in hepatic regucalcin is associated with the development and progression of nonalcoholic fatty liver disease and fibrosis in human patients. Regucalcin may be a key molecule in lipid metabolic disorder and diabetes.
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PMID:Involvement of regucalcin in lipid metabolism and diabetes. 2345 39


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