A high fat, high sugar diet induces hepatic Peroxisome proliferator-activated receptor gamma coactivator 1-alpha promoter hypermethylation in male Wistar rats.

Previously we reported that a high fat, high sugar (HFHS) diet induced adiposity, hyperinsulinaemia, hyperleptinaemia, hypertriglyceridaemia and increased liver mass in male Wistar rats. In the present study, the mechanisms underlying the increased liver mass were further elucidated by assessing hepatic lipid accumulation and the expression and methylation status of key metabolic genes using histology, quantitative real-time PCR and pyrosequencing, respectively. The HFHS diet induced hepatic steatosis, increased hepatic triglycerides (1.

Corrigendum: Characterization of Insulin-Producing β-Cell Spheroids.

[This corrects the article DOI: 10.3389/fcell.2020.

Characterization of Insulin-Producing β-Cell Spheroids.

Over the years, immortalized rodent β-cell lines such as RIN, HIT, MIN, βTC, and INS-1 have been used to investigate pancreatic β-cell physiology using conventional two-dimensional (2D) culture techniques. However, physical and physiological limitations inherent to 2D cell culture necessitates confirmatory follow up studies using sentient animals. Three-dimensional (3D) culture models are gaining popularity for their recapitulation of key features of organ physiology, and thus could pose as potential surrogates for animal experiments.

Hypothalamic neurogenesis and its implications for obesity-induced anxiety disorders.

Obesity and anxiety are public health problems that have no effective cure. Obesity-induced anxiety is also the most common behavioural trait exhibited amongst obese patients, with the mechanisms linking these disorders being poorly understood. The hypothalamus and hippocampus are reciprocally connected, important neurogenic brain regions that could be vital to understanding these disorders.

Linking LOXL2 to Cardiac Interstitial Fibrosis.

Cardiovascular diseases (CVDs) are the leading causes of death worldwide. CVD pathophysiology is often characterized by increased stiffening of the heart muscle due to fibrosis, thus resulting in diminished cardiac function. Fibrosis can be caused by increased oxidative stress and inflammation, which is strongly linked to lifestyle and environmental factors such as diet, smoking, hyperglycemia, and hypertension.

Popular three-dimensional models: Advantages for cancer, Alzheimer's and cardiovascular diseases.

The increasing prevalence of non-communicable diseases, namely cancer, Alzheimer's (AD) and cardiovascular diseases (CVDs), worldwide continues to be a major health burden. Research attempts have been made to understand the pathophysiology and develop effective therapeutic agents for these diseases using conventional in vitro and ex vivo models. Due to the complexity of human disease mechanisms, often these models fail to recapitulate clinically relevant pathologies.

Identification of potential biomarkers for predicting the early onset of diabetic cardiomyopathy in a mouse model.

Type 2 diabetes (T2D) is characterized by metabolic derangements that cause a shift in substrate preference, inducing cardiac interstitial fibrosis. Interstitial fibrosis plays a key role in aggravating left ventricular diastolic dysfunction (LVDD), which has previously been associated with the asymptomatic onset of heart failure. The latter is responsible for 80% of deaths among diabetic patients and has been termed diabetic cardiomyopathy (DCM).

Diet-induced DNA methylation within the hypothalamic arcuate nucleus and dysregulated leptin and insulin signaling in the pathophysiology of obesity.

Obesity rates continue to rise in an unprecedented manner in what could be the most rapid population-scale shift in human phenotype ever to occur. Increased consumption of unhealthy, calorie-dense foods, coupled with sedentary lifestyles, is the main factor contributing to a positive energy balance and the development of obesity. Leptin and insulin are key hormones implicated in pathogenesis of this disorder and are crucial for controlling whole-body energy homeostasis.

In Utero One-Carbon Metabolism Interplay and Metabolic Syndrome in Cardiovascular Disease Risk Reduction.

The maternal obesogenic environment plays a role in programing the susceptibility of the fetus to postnatal non-alcoholic fatty liver disease (NAFLD), a risk factor for cardiovascular disease (CVD). NAFLD is a multisystem disease that is characterized by hepatic fat accumulation due in part to dysregulated energy metabolism network through epigenetic mechanisms such as DNA methylation. DNA methylation affects fetal programing and disease risk via regulation of gene transcription; it is affected by methyl donor nutrients such as vitamin B , methionine, folic acid, vitamin B , and choline.

Diet-induced hypothalamic dysfunction and metabolic disease, and the therapeutic potential of polyphenols.

Background: The prevalence of obesity and metabolic diseases continues to rise globally. The increased consumption of unhealthy energy-rich diets that are high in fat and sugars results in oxidative stress and inflammation leading to hypothalamic dysfunction, which has been linked with these diseases. Conversely, diets rich in polyphenols, which are phytochemicals known for their antioxidant and anti-inflammatory properties, are associated with a reduced risk for developing metabolic diseases.

Repression of and Orthologs in Potato Increases Tuber Starch Bound Phosphate With Concomitant Alterations in Starch Physical Properties.

To examine the roles of starch phosphatases in potatoes, transgenic lines were produced where orthologs of and () were repressed using RNAi constructs. Although repression of either or inhibited leaf starch degradation, it had no effect on cold-induced sweetening in tubers. Starch amounts were unchanged in the tubers, but the amount of phosphate bound to the starch was significantly increased in all the lines, with phosphate bound at the C6 position of the glucosyl units increased in lines repressed in and in the C3 position in lines repressed in expression.