Oligosaccharides improve the flesh quality and nutrition value of Nile tilapia fed with high carbohydrate diet

Abstract Background: Increasing the utilization efficiency of high-carbohydrate diet has the potential to promote “protein sparing effects” in farmed fish; however, many fish utilize carbohydrates poorly. The intestinal microbiota plays an important role in carbohydrate degradation. Whether the addition of functional bacteria could increase the carbohydrate utilization efficiency and alleviate high-carbohydrate diet-induced adverse effects is unknown.Results: A bacterial strain that could degrade starch in vitro was isolated from the intestines of Nile tilapia (Oreochromis niloticus). The bacterium was affiliated to Bacillus amyloliquefaciens (designated as B. amy SS1) based on 16S rRNA gene sequencing. Three diets, including control diet (CON), high-carbohydrate diet (HCD), and high-carbohydrate diet supplemented with B. amy SS1 (HCB), were used to feed Nile tilapia for 10 weeks. The beneficial effects of B. amy SS1 on weight gain and protein accumulation were observed. The HCB decreased blood glucose levels and reduced lipid deposition compared with the HCD group. To detect the possible mechanism, the intestinal microbiota composition was characterized using high-throughput sequencing. The HCB increased the abundance of short-chain fatty acid-producing bacteria. Gas chromatographic analysis indicated that theconcentration of acetate increased dramatically in the HCB group compared with that in the HCD group. Glucagon-like peptide-1 (GLP-1) levels increased in the intestine and serum of the HCB group. Different concentrations of sodium acetate (low (HLA), 900 mg/kg; medium (HMA), 1800 mg/kg, and high (HHA), 3600 mg/kg) were added to the HCD to feed the fish for eight weeks. The HMA and HHA groups mirrored the effects of the HCD supplemented with B. amy SS1 by increasing serum GLP-1 levels. Increased acetate concentrations stimulated GLP-1 production, which might account for the effects caused by the addition of B. amy SS1 to the HCD.Conclusions: This study systematically analyzed the influence of B. amy SS1 on fish metabolism, suggesting that B. amy SS1 treatment alleviates the metabolic syndrome caused by HCD by enriching acetate-producing bacteria in fish intestines. Regulating the intestinal microbiota and their metabolites might represent a powerful strategy for fish nutrition modulation and health maintenance in future.

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Inulin alleviates adverse metabolic syndrome and regulates intestinal microbiota composition in Nile tilapia (Oreochromis niloticus) fed with high-carbohydrate diet

British Journal Of Nutrition ◽

10.1017/s000711452000402x ◽

2020 ◽

pp. 1-11

Author(s):

Tong Wang ◽

Ning Zhang ◽

Xiao-Bo Yu ◽

Fang Qiao ◽

Li-Qiao Chen ◽

...

Keyword(s):

Metabolic Syndrome ◽

Oreochromis Niloticus ◽

Nile Tilapia ◽

Liver Glycogen ◽

Pathogen Resistance ◽

High Carbohydrate Diet ◽

Carbohydrate Diet ◽

Metabolic Characteristics ◽

High Carbohydrate ◽

The Metabolic Syndrome

Abstract A high-carbohydrate diet could achieve a protein-sparing effect, but it may cause negative impacts on the growth condition of fish due to their poor utilisation ability of carbohydrate. How to reduce the adverse effects caused by a high-carbohydrate diet is important for the development of aquaculture. In the present study, we aimed to identify whether inulin could attenuate the metabolic syndrome caused by a high-carbohydrate diet in fish. Nile tilapia (Oreochromis niloticus) (1·19 (sd 0·01) g) were supplied with 35 % carbohydrate (CON), 45 % carbohydrate (HC) and 45 % carbohydrate + 5 g/kg inulin (HCI) diets for 10 weeks. The results showed that addition of inulin improved the survival rate when fish were challenged with Aeromonas hydrophila, indicating that inulin had an immunostimulatory effect. Compared with the HC group, the HCI group had lower lipid accumulation in liver and the gene expression analyses indicated that addition of inulin down-regulated genes related to lipogenesis and up-regulated genes relevant to β-oxidation significantly (P < 0·05). Higher liver glycogen and glucose tolerance were found in the HCI group compared with the HC group (P < 0·05). These results indicated that inulin could alleviate the metabolic syndrome induced by a high-carbohydrate diet. Furthermore, addition of inulin to a high-carbohydrate diet changed the intestinal bacterial composition and significantly increased the concentration of acetic acid and propionic acid in fish gut which have the potential to increase pathogen resistance and regulate metabolic characteristics in fish. Collectively, our results demonstrated a possible causal role for the gut microbiome in metabolic improvements induced by inulin in fish.

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Bacillus amyloliquefaciens ameliorates high-carbohydrate diet-induced metabolic phenotypes by restoration of intestinal acetate-producing bacteria in Nile Tilapia

British Journal Of Nutrition ◽

10.1017/s0007114521001318 ◽

2021 ◽

pp. 1-44

Author(s):

Rong Xu ◽

Miao Li ◽

Tong Wang ◽

Yi-Wei Zhao ◽

Cheng-Jie Shan ◽

...

Keyword(s):

Intestinal Microbiota ◽

Bacillus Amyloliquefaciens ◽

Nile Tilapia ◽

High Carbohydrate Diet ◽

Utilization Efficiency ◽

Fish Nutrition ◽

Carbohydrate Diet ◽

Health Maintenance ◽

Metabolic Phenotypes ◽

High Carbohydrate

Abstract Poor utilization efficiency of carbohydrate always leads to metabolic phenotypes in fish. The intestinal microbiota plays an important role in carbohydrate degradation. Whether the intestinal bacteria could alleviate high-carbohydrate diet (HCD) induced metabolic phenotypes in fish remains unknown. Here, a strain affiliated to Bacillus amyloliquefaciens was isolated from the intestine of Nile tilapia. A basal diet (CON), high carbohydrate diet (HCD), or HCD supplemented with B. amy SS1 (HCB) was used to feed fish for 10 weeks. The beneficial effects of B. amy SS1 on weight gain and protein accumulation were observed. Fasting glucose and lipid deposition were decreased in the HCB group compared with the HCD group. Highthroughput sequencing showed that the abundance of acetate-producing bacteria was increased in the HCB group relative to the HCD group. Gas chromatographic analysis indicated that the concentration of intestinal acetate was increased dramatically in the HCB group compared with that in the HCD group. Glucagon-like peptide-1 (GLP-1) was also increased in the intestine and serum of the HCB group. Thus, fish were fed with HCD, HCD supplemented with sodium acetate at 900 mg/kg (HLA), 1800 mg/kg (HMA) or 3600 mg/kg (HHA) diet for 8 weeks, and the HMA and HHA groups mirrored the effects of B. amy SS1. This study revealed that B. amy SS1 could alleviate the metabolic phenotypes caused by HCD by enriching acetate-producing bacteria in fish intestines. Regulating the intestinal microbiota and their metabolites might represent a powerful strategy for fish nutrition modulation and health maintenance in future.

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

Nutrients ◽

10.3390/nu13072140 ◽

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.

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

Molecules ◽

10.3390/molecules26061638 ◽

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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