A 60-d feeding trial was conducted to explore the potential regulatory effects of dietary Clostridium butyricum cultures (CBC) supplementation in high-carbohydrate diet (HCD) on carbohydrate utilisation, antioxidant capacity and intestinal microbiota of largemouth bass. Triplicate groups of largemouth bass (average weight 35·03 ± 0·04 g), with a destiny of twenty-eight individuals per tank, were fed low-carbohydrate diet and HCD supplemented with different concentration of CBC (0 %, 0·25 %, 0·50 % and 1·00 %). The results showed that dietary CBC inclusion alleviated the hepatic glycogen accumulation induced by HCD intake. Additionally, the expression of hepatic ampkα1 and insulin signaling pathway-related genes (ira, irb, irs, p13kr1 and akt1) increased linearly with dietary CBC inclusion, which might be associated with the activation of glycolysis-related genes (gk, pfkl and pk). Meanwhile, the expression of intestinal SCFA transport-related genes (ffar3 and mct1) was significantly increased with dietary CBC inclusion. In addition, the hepatic antioxidant capacity was improved with dietary CBC supplementation, as evidenced by linear decrease in malondialdehyde concentration and expression of keap1, and linear increase in antioxidant enzyme activities (total antioxidative capacity, total superoxide dismutase and catalase) and expression of antioxidant enzyme-related genes (nrf2, sod1, sod2 and cat). The analysis of bacterial 16S rRNA V3–4 region indicated that dietary CBC inclusion significantly reduced the enrichment of Firmicutes and potential pathogenic bacteria genus Mycoplasma but significantly elevated the relative abundance of Fusobacteria and Cetobacterium. In summary, dietary CBC inclusion improved carbohydrate utilization, antioxidant capacity and intestinal microbiota of largemouth bass fed HCD.

Poor utilisation 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), 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. High-throughput 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 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.

Diet composition and energy content modulate free fatty acid (FFA) release. The aim of this study was to evaluate the dose–response effects of euenergetic variations in dietary carbohydrate and fat content on postabsorptive FFA release. The rate of appearance (Ra) of palmitate was measured by infusion of [2,2-2H2]palmitate after an overnight fast in six healthy men on three separate occasions, i.e. after 7 d on euenergetic control, high-carbohydrate and high-fat diets. The protein content and composition was identical for each diet. Postabsorptive plasma fatty acid concentrations were not different between the high-carbohydrate and control diets (0·36 (SE 0·07) V. 0·43 (se 0·04) mmol/l), but were increased after the high-fat diet (0·75 (se 0·09) mmol/l, (P<0·01 compared with the other diets). Ra palmitate was not different between the high-carbohydrate and control diets (1·36 (se 0·20) v. 1·47 (se 0·15) μmol/kg per min). However, Ra palmitate was increased to 2·36 (se 0·26) μmol/kg per min after the high-fat diet (P<0·01 compared with the other diets). The fatty acid flux and whole-body fat oxidation were not affected by the high-carbohydrate diet compared with the control diet, but were increased by 67 and 47 % respectively, on the high-fat diet (P<0·01 compared with the other diets). A euenergetic high-fat diet results in increased postabsorptive FFA release and fat oxidation, whereas a euenergetic high-carbohydrate diet does not affect these variables of fat metabolism.

There is concern that replacement of dietary fat with carbohydrate may not reduce the overall risk of CHD because this replacement strategy elevates postprandial plasma triacylglycerol (TAG) concentrations. The present study was designed to test the hypothesis that daily exercise can offset the augmented postprandial lipaemia associated with a short-term high-carbohydrate diet. Nine healthy, normolipidaemic men aged 33 (SD 4) YEARS CONSUMED A TEST MEAL (G/KG BODY MASS; 1·2 FAT, 1·1 CARBOHYDRATE, 0·2 PROTEIN) ON THREE OCCASIONS: AFTER 3 D ON A TYPICAL WESTERN DIET (46, 38 AND 16 % ENERGY FROM CARBOHYDRATE, FAT AND PROTEIN RESPECTIVELY); AFTER 3 D ON AN ISOENERGETIC HIGH-CARBOHYDRATE DIET (CORRESPONDING VALUES: 70, 15 AND 15 % ENERGY); AFTER 3 D ON THE SAME HIGH-CARBOHYDRATE DIET WITH 30 MIN MODERATE EXERCISE DAILY. FASTING PLASMA TAG CONCENTRATION WAS HIGHER AFTER THE HIGH-CARBOHYDRATE DIET (1·15 (se 0·16) mmol/l) than after the Western diet (0·83 (se 0·10) mmol/l; P=0·03). Similarly, postprandial lipaemia (6 h total area under plasma TAG concentration v. time curve) was higher after the high-carbohydrate diet (12·54 (se 2·07) mmol/l·h) than after the Western diet (9·30 (se 1·30) mmol/l·h; P=0·004). The addition of exercise to the high-carbohydrate diet significantly reduced postprandial lipaemia (9·95 (se 1·94) mmol/l·h; P=0·01 when compared with the high-carbohydrate diet) but not fasting TAG concentration (1·02 (se 0·24) mmol/l). In conclusion, daily exercise prevented the augmentation of postprandial lipaemia attributable to the short-term high-carbohydrate diet and, thus, exercise may be a powerful adjunct to dietary change.

Using cytofluorimetric and biochemical methods, the content of glycogen and its labile and stable fractions, as well as activities of glucose-6-phosphatase (EC 3.1.3.9), glycogen phosphorylase (EC 2.4.1.1) and glycogen synthase (EC 2.4.1.11) were determined in the rat liver for 6 months after chronic poisoning of the animals with CCl4 and then at 1, 3, and 6 months after the end of the poisoning. One group of rats was given a standard diet, the other, a high-carbohydrate diet. The 6-month long chronic intoxication with CCl4 was shown to produce development of typical liver cirrhosis characterized by a 2·8-fold increase in the total glycogen content in hepatocytes as compared with normal cells, by a fall in the glycogen labile fraction (from 85 to 53 % of the total glycogen) as well as by decreases in the activities of glycogen phosphorylase and glucose-6-phosphatase by 25 and 82% respectively. The structural rehabilitation occurred faster and more completely at the cellular level than at the tissue level. Functional variables of the cirrhotic liver tissue also recovered, after cessation of poisoning, faster and more completely than the liver structure at the tissue level: glycogen levels in hepatocytes fell dramatically, the labile: stable glycogen fraction ratio recovered completely, and the activity of glycogen phosphorylase rose to the level characteristic of the normal liver. Use of the high-carbohydrate diet promoted a somewhat faster and more complete recovery of hepatic structure and function.

Glycogen synthase (GS) activity was characterized in rat brown adipose tissue (BAT) and the activity was found to be much higher than that in white adipose tissue. Prolonged starvation had no effect on the active form of GS, as found in the liver and muscle. The GS activity was similar in BAT of rats housed in an animal room (21+± 1°) whether they were fed on high-carbohydrate, high-fat, or stock diets. Acclimatizatioin of rats to cold (4+± 1°) for 2 weeks significantly increased GS activity. This increase in the cold was fivefold greater when rats were fed on high-carbohydrate diets than in control rats at room temperature fed on an identical diet. The increase was accompanied by a large accumulation of glycogen in BAT. It was concluded that GS may play an important role in BAT and may contribute to the control of blood glucose in a cold environment. Its relevance to thermogenesis requires further elucidation.