Exploring Bile-Acid Changes and Microflora Profiles in Chicken Fatty Liver Disease Model.

Excessive liver fat causes non-alcoholic fatty liver disease (NAFLD) in laying hens, reducing egg production. Addressing NAFLD via bile-acid metabolism is gaining attention. We induced NAFLD in 7-week-old ISA female chickens with a high-cholesterol, low-choline diet (CLC) for 6 weeks.

Targeting an allosteric site in dynamin-related protein 1 to inhibit Fis1-mediated mitochondrial dysfunction.

The large cytosolic GTPase, dynamin-related protein 1 (Drp1), mediates both physiological and pathological mitochondrial fission. Cell stress triggers Drp1 binding to mitochondrial Fis1 and subsequently, mitochondrial fragmentation, ROS production, metabolic collapse, and cell death. Because Drp1 also mediates physiological fission by binding to mitochondrial Mff, therapeutics that inhibit pathological fission should spare physiological mitochondrial fission.

Drp1/p53 interaction mediates p53 mitochondrial localization and dysfunction in septic cardiomyopathy.

Background: Previous studies have implicated p53-dependent mitochondrial dysfunction in sepsis induced end organ injury, including sepsis-induced myocardial dysfunction (SIMD). However, the mechanisms behind p53 localization to the mitochondria have not been well established. Dynamin-related protein 1 (Drp1), a mediator of mitochondrial fission, may play a role in p53 mitochondrial localization.

Early-onset caloric restriction alleviates ageing-associated steatohepatitis in male mice via restoring mitochondrial homeostasis.

Non-alcoholic fatty liver disease is associated with ageing, and impaired mitochondrial homeostasis is the main cause for hepatic ageing. Caloric restriction (CR) is a promising therapeutic approach for fatty liver. The purpose of the present study was to investigate the possibility of early-onset CR in decelerating the progression of ageing-related steatohepatitis.

Long-term dietary restriction ameliorates ageing-related renal fibrosis in male mice by normalizing mitochondrial functions and autophagy.

As the kidneys age, gradual changes in the structures and functions of mitochondria occur. Dietary restriction (DR) can play a protective role in ageing-associated renal decline, however the exact mechanisms involved are still unclear. This study aims to clarify the beneficial effects of long-term DR on renal ageing and to explore the potential mechanisms of mitochondrial homeostasis.

ALDH2 Expression, Alcohol Intake and Semen Parameters among East Asian Men.

Purpose: Inactivating mutations in mitochondrial aldehyde dehydrogenase 2 (ALDH2) are highly prevalent. The most common variant allele, , is present in 40%-50% of East Asians, and causes acetaldehyde accumulation, flushing and tachycardia after alcohol intake. The relationship between alcohol intake and ALDH2 genotype on semen parameters remains unknown.

Early-onset dietary restriction maintains mitochondrial health, autophagy and ER function in the left ventricle during aging.

Dietary restriction (DR) exerts healthy benefits, including heart functions. However, the cardioprotective role of DR is till controversial among researchers due to the variation of DR conditions. The present study focuses on the protective effect of early-onset DR on cardiac injury using mitochondrial structure and expression of protein associated with mitochondrial homeostasis, autophagy and endoplasmic reticulum (ER) function as measures.

Determination of mitochondrial functions and damage in kidney in female LeeSung minipigs with a high-fat diet-induced obesity.

The purpose of this study was to investigate the nexus between mitochondrial function and kidney injury by using a dietary-induced obese minipig model. Female Lee-Sung minipigs feeding a high-fat diet (HFD) for 6 months exhibited obesity, hyperglycaemia and dyslipidemia. HFD elevated the levels of plasma biomarkers related to renal injury, including symmetric dimethylarginine, creatinine and urea nitrogen.

Novel and prevalent non-East Asian ALDH2 variants; Implications for global susceptibility to aldehydes' toxicity.

Background: Aldehyde dehydrogenase 2 (ALDH2) catalyzes the detoxification of aliphatic aldehydes, including acetaldehyde. About 45% of Han Chinese (East Asians), accounting for 8% of humans, carry a single point mutation in ALDH2*2 (E504K) that leads to accumulation of toxic reactive aldehydes.

Methods: Sequencing of a small Mexican cohort and a search in the ExAC genomic database for additional ALDH2 variants common in various ethnic groups was set to identify missense variants.

The impact of DRP1 on myocardial fibrosis in the obese minipig.

Background: The heart is a highly oxidative tissue, thus mitochondria play a major role in maintaining optimal cardiac function. Our previous study established a dietary-induced obese minipig with cardiac fibrosis. The aim of this study was to elucidate the role of mitochondrial dynamics in cardiac fibrosis of obese minipigs.

Involvement of pericardial adipose tissue in cardiac fibrosis of dietary-induced obese minipigs- Role of mitochondrial function.

Background: Heart is a high energy demand organ and cardiac fat is the main local energy source for heart. Alteration in cardiac fat may affect cardiac energy and contribute to heart dysfunction. We previously observed a link between alteration in pericardial fat (PAT) and local adverse effects on myocardial fibrosis in obese minipigs.

The role of pericardial adipose tissue in the heart of obese minipigs.

Background: Pericardial adipose tissue (PAT) volume is highly associated with the presence and severity of cardiometabolic diseases, but the underlying mechanism is unknown. We previously demonstrated that a high-fat diet (HFD) induced metabolic dysregulation, cardiac fibrosis and accumulation of more PAT in minipigs. This study used our obese minipig model to investigate the characteristics of PAT and omental visceral fat (VAT) induced by a HFD, and the potential link between PAT and HFD-related myocardial fibrosis.

Eicosapentaenoic acid protects cardiomyoblasts from lipotoxicity in an autophagy-dependent manner.

Background And Aims: The cardiovascular health benefits of eicosapentaenoic acid (EPA) have been demonstrated previously; however, the exact mechanism underlying them remains unclear. Our previous study found that lipotoxicity induced cardiomyocyte apoptosis via the inhibition of autophagy. Accordingly, in this study, we investigated whether EPA attenuated lipotoxicity-induced cardiomyocyte apoptosis through autophagy regulation.

The high-fat diet induces myocardial fibrosis in the metabolically healthy obese minipigs-The role of ER stress and oxidative stress.

Background: The cellular mechanisms of obesity-induced cardiomyopathy are multiple and not completely elucidated. The objective of this study was to differentiate two obesity-associated cardiomyopathy miniature pig models: one with the metabolic syndrome (MetS), and one with a metabolically healthy obesity (MHO). The cellular responses during the development of obesity-induced cardiomyopathy were investigated.

A nutritional nonalcoholic steatohepatitis minipig model.

Background And Aims: The objective of this study was to elucidate whether a Western diet was associated with nonalcoholic steatohepatitis (NASH), and the relationship between NASH, autophagy and endoplasmic reticulum (ER) stress.

Methods: Four-month-old Lee-Sung minipigs were randomly assigned to two groups: control diet (C) and Western diet (W), for a 5-month experimental period.

Results: Feeding a Western diet produced a body composition with more fat, less lean and a greater liver weight.

Time-dependent cellular response in the liver and heart in a dietary-induced obese mouse model: the potential role of ER stress and autophagy.

Purpose: Both endoplasmic reticulum stress (ER stress) and autophagy are essential for the response of the protein quality control system to cellular stresses. This study investigated the influence of the duration of a high-fat diet (HFD) in mice on tissue-specific cellular responses, specifically with regard to the role of autophagy and ER stress.

Methods: Male mice aged 6-7 weeks were fed ad libitum with a standard chow diet or with a HFD for 2, 4, 8, or 16 weeks.

Development of a dietary-induced metabolic syndrome model using miniature pigs involvement of AMPK and SIRT1.

Background: During the progression of the metabolic syndrome (MetS), cardiovascular diseases (CVD) appear clinically in many individuals and cause death. As a result, it is essential to set up an optimal animal model to study the mechanism of MetS leading to CVD. SIRT1 and AMPK are the master regulators of lipid and carbohydrate metabolism.