Nonalcoholic fatty liver disease: a marker of adipose tissue distribution

Recent evidence has shifted the paradigm of white adipose tissue from simple energy storage to the body's major endocrine and paracrine organ synthesizing and releasing multiple signaling proteins, collectively termed adipokines. White adipose tissue is distributed in two large depots (subcutaneous and visceral) and many small depots associated with the heart, blood vessels, lymph nodes, ovaries, mammary glands, prostate gland, pancreas. Even in a lean person, adipose tissue represents about 15-20 % of body weight, including external (subcutaneous and visceral) and internal (organ-associated) adipose tissue, the latter being even more important than the former; however the internal fat distribution was beyond the scope of the present study. Nonalcoholic fatty liver disease (NAFLD) is a term used to describe the accumulation of fat in the liver of people in the absence of alcohol consumption or consumption of less than 20 g/day. It is a progressive, low-grade inflammatory disease related to obesity and metabolic syndrome. NAFLD represent a spectrum of disorders ranging from fat accumulation (steatosis) to nonalcoholic steatohepatitis (NASH) that can progress to fibrosis and cirrhosis. The aim of the present study was to evaluate the clinic and metabolic parameters in patients with type 2 diabetes and NAFLD depending on gender and BMI and to assess relation of adipose tissue distribution with insulin resistance. Total of 118 patients (mean age 55.93 years; male, 46, female, 72) with type 2 diabetes evaluated in an outpatient diabetes clinic were diagnosed with NAFLD by ultrasonography and were assessed by weight, body mass index (BMI), waist circumference, fasting plasma glucose, HbAlc, and fasting insulin level. We calculated the HOMA-IR index [FPG (mmol/l) x FI (μU/ml)]:22.5. Body adipose percentage and trunk adipose content were measured using bioelectrical impedance analysis (TANITA BC-418). Overall, the present results suggest that insulin resistance may be considered a pathogenic link between T2DM and NAFLD, also at the level of adipose tissue distribution. Evaluating the distribution of internal, organ-associated adipose tissue remains a challenge for future studies in patients with T2DM and NAFLD.Adipobiology 2012; 4: 97-101

Design and baseline characteristics of the finerenone in reducing cardiovascular mortality and morbidity in diabetic kidney disease trial

Background: Among people with diabetes, those with kidney disease have exceptionally high rates of cardiovascular (CV) morbidity and mortality and progression of their underlying kidney disease. Finerenone is a novel, nonsteroidal, selective mineralocorticoid receptor antagonist that has shown to reduce albuminuria in type 2 diabetes (T2D) patients with chronic kidney disease (CKD) while revealing only a low risk of hyperkalemia. However, the effect of finerenone on CV and renal outcomes has not yet been investigated in long-term trials. Patients and Methods: The Finerenone in Reducing CV Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD) trial aims to assess the efficacy and safety of finerenone compared to placebo at reducing clinically important CV and renal outcomes in T2D patients with CKD. FIGARO-DKD is a randomized, double-blind, placebo-controlled, parallel-group, event-driven trial running in 47 countries with an expected duration of approximately 6 years. FIGARO-DKD randomized 7,437 patients with an estimated glomerular filtration rate >= 25 mL/min/1.73 m(2) and albuminuria (urinary albumin-to-creatinine ratio >= 30 to <= 5,000 mg/g). The study has at least 90% power to detect a 20% reduction in the risk of the primary outcome (overall two-sided significance level alpha = 0.05), the composite of time to first occurrence of CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. Conclusions: FIGARO-DKD will determine whether an optimally treated cohort of T2D patients with CKD at high risk of CV and renal events will experience cardiorenal benefits with the addition of finerenone to their treatment regimen. Trial Registration: EudraCT number: 2015-000950-39; ClinicalTrials.gov identifier: NCT02545049