Effects of a high-fat and high-carbohydrate diet on appetite regulation and central AMPK in the hypothalamus of blunt snout bream (Megalobrama amblycephala).

Adenosine monophosphate-activated protein kinase (AMPK) is a sensor of cellular energy changes and controls food intake. This study investigates the effect of a high-calorie diet (high fat diet [HFD], high carbohydrate diet [HCD] and high energy diet [HED]) on appetite and central AMPK in blunt snout bream. In the present study, fish (average initial weight 45.84 ± 0.07 g) were fed the control, HFD, HCD and HED in four replicates for 12 weeks. At the end of the feeding trial, the result showed that body mass index, specific growth rate, feed efficiency ratio and feed intake were not affected (p > 0.05) by dietary treatment. However, fish fed the HFD obtained a significantly higher (p < 0.05) lipid productive value, lipid gain and lipid intake than those fed the control diet, but no significant difference was attributed to others. Also, a significantly higher (p < 0.05) energy intake content was found in fish-fed HFD, HCD and HED than those given the control diet. Long-term HFD and HCD feeding significantly increased (p < 0.05) plasma glucose, glycated serum protein, advanced glycation end product, insulin and leptin content levels than the control group. Moreover, a significantly lower (p < 0.05) complex 1, 2 and 3 content was found in fish-fed HFD and HCD than in the control, but no differences (p > 0.05) were attributed to those in HED. Fish-fed HED significantly upregulated (p < 0.05) hypothalamic ampα 1 and ampα 2 expression, whereas the opposite trend was observed in the hypothalamic mammalian target of rapamycin than those in HFD and HCD compared to the control. However, hypothalamic neuropeptide y, peroxisome proliferator-activated receptor α (pparα), acetyl-coa oxidase and carnitine palmitoyltransferase 1 were significantly upregulated (p < 0.05) in the HCD group, while the opposite was seen in cholecystokinin expression compared to those in the control group. Our findings indicated that the central AMPK signal pathway and appetite were modulated according to the diet's energy level to regulate nutritional status and maintain energy homoeostasis in fish.

High-fat diet alters intestinal microbiota and induces endoplasmic reticulum stress via the activation of apoptosis and inflammation in blunt snout bream.

The primary organ for absorbing dietary fat is the gut. High dietary lipid intake negatively affects health and absorption by causing fat deposition in the intestine. This research explores the effect of a high-fat diet (HFD) on intestinal microbiota and its connections with endoplasmic reticulum stress and inflammation. 60 fish (average weight: 45.84 ± 0.07 g) were randomly fed a control diet (6% fat) and a high-fat diet (12 % fat) in four replicates for 12 weeks. From the result, hepatosomatic index (HSI), Visceralsomatic index (VSI), abdominal fat (ADF), Intestosomatic index (ISI), mesenteric fat (MFI), Triglycerides (TG), total cholesterol (TC), non-esterified fatty acid (NEFA) content were substantially greater on HFD compared to the control diet. Moreover, fish provided the HFD significantly obtained lower superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. In contrast, an opposite result was seen in malondialdehyde (MDA) content in comparison to the control. HFD significantly altered intestinal microbiota in blunt snout bream, characterized by an increased abundance of Aeromonas, Plesiomonas proteobacteria, and firmicutes with a reduced abundance of Cetobacterium and ZOR0006. The transcriptional levels of glucose-regulated protein 78 (grp78), inositol requiring enzyme 1 (ire1), spliced X box-binding protein 1 (xbp1), DnaJ heat shock protein family (Hsp40) member B9 (dnajb9), tumor necrosis factor alpha (tnf-α), nuclear factor-kappa B (nf-κb), monocyte chemoattractant protein-1 (mcp-1), and interleukin-6 (il-6) in the intestine were markedly upregulated in fish fed HFD than the control group. Also, the outcome was similar in bax, caspases-3, and caspases-9, ZO-1, Occludin-1, and Occludin-2 expressions. In conclusion, HFD could alter microbiota and facilitate chronic inflammatory signals via activating endoplasmic reticulum stress.

Evaluation of antioxidant capacity and immunomodulatory effects of yeast hydrolysates for hepatocytes of blunt snout bream (Megalobrama amblycephala).

An in-vitro study was carried out to examine the effects of yeast hydrolysate (YH) on antioxidant capacity and innate immunity of blunt snout bream (Megalobrama amblycephala) hepatocytes. Fish primary hepatocytes were seeded at a density of 3 × 105 cells mL-1 in 6-well tissue culture plates and treated with two different media including: 1) DMEM/F12 medium (control), and 2) YH medium [DMEM/F12 + 0.1 g L-1 YH]. After incubation for 24 h, the culture medium and primary hepatocytes were collected for subsequent analyses. The results showed no significant (P > 0.05) effect of YH on aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activities and urea nitrogen (UN) concentration in the conditioned medium. However, significantly (P < 0.05) higher ALT and AST activities were found in YH treated hepatocytes compared to control. Moreover, YH supplementation led to significant enhancement of superoxide dismutase (SOD), catalase (CAT), alternative complement pathway (ACH50) and glutathione peroxidase (GPX) activities and reduction of malondialdehyde (MDA) concentration in the conditioned medium. Furthermore, YH application upregulated the expression of SOD, CAT and NOX2 genes and downregulated mRNA levels of Keap1, Nrf2 and Bach1 in hepatocytes. Also, markedly higher lysozyme activity and albumin concentration were found in the conditioned medium of YH group compared to the control. Additionally, expression of immune-related genes such as antimicrobial peptides 1 (Leap 1) and Leap 2 were significantly upregulated by YH application. Down-regulated expression of NADPH oxidase-2 (NOX2), Kelch-like-ECH-associated protein 1 (Keap1), NF-E2-related factor 2 (Nrf2) and BTB and CNC homolog 1 (Bach1) were observed in YH treated hepatocytes. To conclude, YH supplementation improved antioxidant capacity and innate immunity of blunt snout bream hepatocytes.

Influences of glycyrrhetinic acid (GA) dietary supplementation on growth, feed utilization, and expression of lipid metabolism genes in channel catfish (Ictalurus punctatus) fed a high-fat diet.

An 8-week feeding trial was performed to test the effects of glycyrrhetinic acid (GA) on growth and some gene expression of hepatic lipid metabolism in channel catfish (initial body weight, 3.5 ± 0.02 g) fed high-fat diets. Fish were fed the control diet, high-fat diet (HFD), and HFD supplemented with 0.4, 0.8, and 1.2 mg/kg GA in 15 tanks at a stocking density of 21 fish/tank. Fish fed HFD were significantly lower in body weight gain and specific growth rate but higher in feed intake and feed conversion ratio in comparison to the control. Supplement of GA at 1.2 mg/kg remarkably improved these parameters as compared to the control diet. High levels of cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), and low levels of high-density lipoprotein (HDL) in plasma were observed in fish fed HFD; the opposite was observed for fish fed HFD supplemented with GA. The transcription of fatty acid synthase (FAS), sterol regulatory element-binding protein-1 (SREBP1), liver X receptor alpha (LXRα), and hormone-sensitive lipase (HSL) was upregulated, while that of carnitine palmitoyltransferase I (CPT1), peroxisome proliferator-activated receptors alpha (PPARα), acyl-CoA oxidase (ACO), and microsomal triglyceride transfer protein (MTTP) mRNA expression were downregulated in fish fed HFD. The opposite was observed in fish fed HFD supplemented with GA as well as the control group. In conclusion, supplementing the HFD with GA at 1.2 mg/kg could improve the growth performance and lipid metabolism of channel catfish consuming HFD.