1,721,135 research outputs found
Not all fats are created equal: adipose vs. ectopic fat, implication in cardiometabolic diseases
No full textAdipose tissue is a recognized endocrine organ that acts not only as a fuel storage but also is able to secrete adipokines that can modulate inflammation. Most of the fat is composed of white adipocytes (WAT), although also brown/beige adipocytes (BAT/BeAT) have been found in humans. BAT is located close to the neck but also among WAT in the epicardial fat and perivascular fat. Adipocyte hypertrophy and infiltration of macrophages impair adipose tissue metabolism determining "adiposopathy" (i.e., sick fat) and increasing the risk to develop metabolic and cardiovascular diseases. The purpose of this review was to search and discuss the available literature on the impact of different types of fat and fat distribution on cardiometabolic risk. Visceral fat, but also ectopic fat, either in liver, muscle and heart, can increase the risk to develop insulin resistance, type 2 diabetes and cardiovascular diseases. Results recently published showed that BAT could have an impact on cardiometabolic risk, not only because it is implicated in energy metabolism but also because it can modulate glucose and lipid metabolism. Therapeutical interventions that can increase energy expenditure, successfully change fat distribution and reduce ectopic fat, also through BAT activation, were discussed
Nonalcoholic Fatty Liver Disease and Type 2 Diabetes: Common Pathophysiologic Mechanisms
No full textNonalcoholic fatty liver disease (NAFLD) is an independent risk factor for advanced liver disease, type 2 diabetes (T2DM), and cardiovascular diseases. The prevalence of NAFLD in the general population is around 30 %, but it is up to three times higher in those with T2DM. Among people with obesity and T2DM, the NAFLD epidemic also is worsening. Therefore, it is important to identify early metabolic alterations and to prevent these diseases and their progression. In this review, we analyze the pathophysiologic mechanisms leading to NAFLD, particularly, those common to T2DM, such as liver and muscle insulin resistance. However, it is mainly adipose tissue insulin resistance that results in increased hepatic de novo lipogenesis, inflammation, and lipotoxicity. Although genetics predispose to NAFLD, an unhealthy lifestyle, including high-fat/high-sugar diets and low physical activity, increases the risk. In addition, alterations in gut microbiota and environmental chemical agents, acting as endocrine disruptors, may play a role
Modeling interpretation of microbe metabolism detected by nuclear magnetic resonance
No full textA new modeling approach is discussed for the analysis of microbial dynamics. It is based on structurally
nonlinear compartmental models and on the dynamics of the substrate and product. Experimental data were
acquired by NMR spectroscopy which is a noninvasive technique. This combined approach was tested with
the fermentation of glucose to ethanol by Saccharomyces cerevisiae. The model was fitted with the experimental
data to obtain the values of the parameters of the model. Similar processes can be analyzed and
compared using this approach
The Subtle Balance between Lipolysis and Lipogenesis: A Critical Point in Metabolic Homeostasis
No full textExcessive accumulation of lipids can lead to lipotoxicity, cell dysfunction and alteration in metabolic pathways, both in adipose tissue and peripheral organs, like liver, heart, pancreas and muscle. This is now a recognized risk factor for the development of metabolic disorders, such as obesity, diabetes, fatty liver disease (NAFLD), cardiovascular diseases (CVD) and hepatocellular carcinoma (HCC). The causes for lipotoxicity are not only a high fat diet but also excessive lipolysis, adipogenesis and adipose tissue insulin resistance. The aims of this review are to investigate the subtle balances that underlie lipolytic, lipogenic and oxidative pathways, to evaluate critical points and the complexities of these processes and to better understand which are the metabolic derangements resulting from their imbalance, such as type 2 diabetes and non alcoholic fatty liver disease
Phthalates exposure as determinant of albuminuria in type 2 diabetes subjects: a cross-sectional study
No full textCONTEXT: Recent epidemiological observations have reported an association among phthalates exposure and insulin resistance, obesity, and diabetes but have not related exposure to these environmental pollutants with microvascular complications of diabetes. OBJECTIVE: To explore the relationship between phthalates and renal function in subjects with diabetes. DESIGN: Cross-sectional, case-only study. Concentrations of three urinary metabolites of di-2-ethylhexylphthalate were quantified in a spot morning urine sample, normalized for creatinine urinary excretion, and related to clinical parameters and phenotype, adjusting for confounders. PATIENTS: Two hundred and nine patients with diabetes consecutively referred to our clinic. MAIN OUTCOME MEASURES: Relationship between phthalates and renal function [evaluated with estimated glomerular filtration rate (eGFR) and albuminuria]. RESULTS: Creatinine-adjusted urinary concentrations of mono-2-ethylhexyl phthalate (MEHP), mono-2-ethyl-5-oxohexyl phthalate (MEOHP), and mono-2-ethyl-5-hydroxyhexyl phthalate were 7.53 μg/g (range, 4.84 to 12.60), 3.04 μg/g (range, 1.03 to 5.14), and 10.70 μg/g (7.02 to 17.40), respectively. Age, sex, body mass index, diabetes duration, smoking, blood pressure, glycated Hb, and eGFR did not influence their levels. Exposure to MEHP and MEOHP was greater in individuals with microalbuminuria/macroalbuminuria (MEHP, P = 0.0173; MEOHP, P = 0.0306). The fourth vs first quartile showed a greater risk of albuminuria (MEHP: OR, 4.83; 95% CI, 1.45 to 16.06; P = 0.0297; MEOHP: OR, 3.29; 95% CI, 1.08 to 10.04); P = 0.0352). MEOHP was greater (P = 0.034) in subjects with cardiovascular events; MEHP showed a positive trend (P = 0.061). CONCLUSION: Our findings have revealed an association between exposure to di-2-ethylhexylphthalate metabolites and the degree of albuminuria in subjects with diabetes; the lack of a relationship with eGFR suggests their urinary levels are independent of renal function
Assessment of RANKL/RANK/osteoprotegerin system expression in patients with hepatocellular carcinoma
No full text
Early increase in N(epsilon)-carboxy-methyl-lysine and decrease in sRAGE plasma values in de novo liver transplantation
No full textBackground: Advanced glycation end-products (AGEs) – such as the N(epsilon)-carboxy-methyl-lysine,CML) - and the soluble form of receptor for AGEs (sRAGE) have been reported as emerging biomarker in cardiovascular, metabolic and inflammatory diseases. Their behavior in the setting of liver transplantation (LT) is poorly understood.
Methods: Seventeen patients undergoing LT were included in a prospective study. CML and sRAGE were determined before LT, after graft reperfusion and 1, 2, 7 ,30 and 90 days after LT.
Results: Baseline CML plasma levels decreased after graft reperfusion (15.7±4.6and8.8±2.7 μg/mL, before LT and after graft reperfusion, respec tively) while returned progressively to baseline values during the follow-up (15.1±5.6 μg/mL at 90 days after LT) (ANOVA, p < 0.0001).The plasma levels of sRAGE did not change significantly soon after LT (median: 872, 1277, 1310, 835pg/mL, before LT, after graft reperfusion, 1 and 2 days after LT, respectively), while they decreased from the seventh day after LT and remained constantly low during the follow-up (274,391 and 233pg/mL, respectively 7, 30 and 90 days after OLT ) (ANOVA, p < 0.0001).
Conclusions: Our study provides further evidence to the role of the liver in the metabolism and/or clearance o fCML, while the early decline of sRAGE might be accounted for by use of immunosuppressive medication. CML accumulation and decrease of protective titers of sRAGE might account for the negative metabolic impact of immunosuppression in the setting of LT and be of relevance to current clinical practice
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