scholarly journals Transcriptomics, metabolomics and histology indicate that high-carbohydrate diet negatively affects the liver health of blunt snout bream (Megalobrama amblycephala)

BMC Genomics ◽  
2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Wassana Prisingkorn ◽  
Panita Prathomya ◽  
Ivan Jakovlić ◽  
Han Liu ◽  
Yu-Hua Zhao ◽  
...  
Keyword(s):  
High Carbohydrate Diet ◽  
Megalobrama Amblycephala ◽  
Carbohydrate Diet ◽  
Blunt Snout Bream ◽  
High Carbohydrate ◽  
Liver Health

Gene expression patterns indicate that a high-fat–high-carbohydrate diet causes mitochondrial dysfunction in fish

Genome ◽  
2019 ◽  
Vol 62 (2) ◽  
pp. 53-67
Author(s):  
Wassana Prisingkorn ◽  
Ivan Jakovlić ◽  
Shao-Kui Yi ◽  
Fang-Yu Deng ◽  
Yu-Hua Zhao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Expression Patterns ◽  
Nutrient Utilization ◽  
High Carbohydrate Diet ◽  
Megalobrama Amblycephala ◽  
High Fat ◽  
Carbohydrate Diet ◽  
High Carbohydrate

Expensive and unsustainable fishmeal is increasingly being replaced with cheaper lipids and carbohydrates as sources of energy in aquaculture. Although it is known that the excess of lipids and carbohydrates has negative effects on nutrient utilization, growth, metabolic homeostasis, and health of fish, our current understanding of mechanisms behind these effects is limited. To improve the understanding of diet-induced metabolic disorders (both in fish and other vertebrates), we conducted an eight-week high-fat–high-carbohydrate diet feeding trial on blunt snout bream (Megalobrama amblycephala), and studied gene expression changes (transcriptome and qPCR) in the liver. Disproportionately large numbers of differentially expressed genes were associated with mitochondrial metabolism, neurodegenerative diseases (Alzheimer’s, Huntington’s, and Parkinson’s), and functional categories indicative of liver dysfunction. A high-fat–high-carbohydrate diet may have caused mitochondrial dysfunction, and possibly downregulated the mitochondrial biogenesis in the liver. While the relationship between diet and neurodegenerative disorders is well-established in mammals, this is the first report of this connection in fish. We propose that fishes should be further explored as a potentially promising model to study the mechanisms of diet-associated neurodegenerative disorders in humans.

scholarly journals High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2140
Author(s):  
Yumiko Takahashi ◽  
Yutaka Matsunaga ◽  
Hiroki Yoshida ◽  
Terunaga Shinya ◽  
Ryo Sakaguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transporter ◽  
High Carbohydrate Diet ◽  
Oral Glucose ◽  
Carbohydrate Diet ◽  
Post Exercise ◽  
Glucose Administration ◽  
Protein Levels ◽  
High Carbohydrate ◽  
Glucose Transporter 2

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

scholarly journals Improvement of Obesity and Dyslipidemic Activity of Amomum tsao-ko in C57BL/6 Mice Fed a High-Carbohydrate Diet

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1638
Author(s):  
Ju-Hyoung Park ◽  
Eun-Kyung Ahn ◽  
Min Hee Hwang ◽  
Young Jin Park ◽  
Young-Rak Cho ◽  
...  
Keyword(s):  
Body Weight Gain ◽  
Subcutaneous Fat ◽  
Density Lipoprotein ◽  
Ethanol Extract ◽  
Cardiac Risk ◽  
Normal Diet ◽  
High Carbohydrate Diet ◽  
Atherogenic Index ◽  
Carbohydrate Diet ◽  
High Carbohydrate

Amomum tsao-ko Crevost et Lemaire (Zingiberaceae) is a medicinal herb found in Southeast Asia that is used for the treatment of malaria, abdominal pain, dyspepsia, etc. The aim of this study was to investigate the effect of an ethanol extract of Amomum tsao-ko (EAT) on obesity and hyperlipidemia in C57BL/6 mice fed a high-carbohydrate diet (HCD). First, the mice were divided into five groups (n = 6/group) as follows: normal diet, HCD, and HCD+EAT (100, 200, and 400 mg/kg/day), which were orally administered with EAT daily for 84 days. Using microcomputed tomography (micro-CT) analysis, we found that EAT inhibited not only body-weight gain, but also visceral fat and subcutaneous fat accumulation. Histological analysis confirmed that EAT decreased the size of fat tissues. EAT consistently improved various indices, including plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein, high-density lipoprotein, atherogenic index, and cardiac risk factors, which are related to dyslipidemia—a major risk factor for heart disease. The contents of TC and TG, as well as the lipid droplets of HCD-induced hepatic accumulation in the liver tissue, were suppressed by EAT. Taken together, these findings suggest the possibility of developing EAT as a therapeutic agent for improving HCD-induced obesity and hyperlipidemia.

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