Resveratrol Improves the Energy Sensing and Glycolipid Metabolism of Blunt Snout Bream Megalobrama amblycephala Fed High-Carbohydrate Diets by Activating the AMPK–SIRT1–PGC-1α Network

Abstract

This study investigated the effects of resveratrol on the growth performance, energy sensing, glycolipid metabolism and glucose and insulin load of blunt snout bream Megalobrama amblycephala fed high-carbohydrate diets. Fish (39.44 ± 0.06 g) were randomly fed three diets: a control diet (30% carbohydrate), a high-carbohydrate diet (HC, 41% carbohydrate), and the HC diet supplemented with 0.04% resveratrol (HCR) for 12 weeks. Fish fed the HC diet had significantly high values of nitrogen and energy retention efficiency, hepatosomatic index, intraperitoneal fat ratio, whole-body lipid content and intraperitoneal fat glycogen and lipid contents compared to the control group, but showed little difference with the HCR treatment. Liver and muscle lipid contents and plasma levels of glucose, glycated serum protein, advanced glycation end products and total cholesterol of fish fed the HC diet were significantly higher than those of the control group, whereas the opposite was found with resveratrol supplementation. Fish fed the HC diet obtained significantly low values of plasma insulin levels and hepatic adenosine monophosphate (AMP) contents and NAD+/NADH ratio compared to HCR treatment, but showed little difference with the control group. The opposite was found for hepatic adenosine triphosphate (ATP) contents and the ATP/AMP ratio. In addition, fish fed the HC diet showed significantly high transcriptions of glucose transporter 2 (GLUT2), glucose-6-phosphate dehydrogenase, glycogen synthase, fatty acid synthetase (FAS), acetyl-CoA carboxylase α (ACCα), peroxisome proliferator-activated receptor γ and PPARα compared to the control group, whereas the opposite was found for protein levels of AMP-activated protein kinase α (t-AMPKα), phosphorylated AMP-activated protein kinase α (p-AMPKα), sirtuin-1 (SIRT1), and p-AMPKα/t-AMPKα ratio as well as the transcriptions of AMPKα1, AMPKα2, SIRT1, PPARγ coactivator-1α (PGC-1α), phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase (FBPase), glucose-6-phosphatase, carnitine palmitoyl transferase I (CPT I) and acyl-CoA oxidase. Resveratrol supplementation significantly up-regulated the protein levels of t-AMPK, p-AMPK, and SIRT1, p-AMPK/t-AMPK ratio as well as the transcriptions of AMPKα1, AMPKα2, SIRT1, PGC-1α, GLUT2, FBPase, and CPT I compared to HC group, while the opposite was found for sterol regulatory element-binding protein-1, FAS and ACCα. Furthermore, resveratrol improved glucose and insulin tolerance of fish fed the HC diet after glucose and insulin load.

Potential role of mitochondria in gastric cancer detection: Fission and glycolysis (Review)

“…AMPK, another key energy metabolic sensor, plays a key role in maintaining cellular energy homeostasis and is activated upon alterations in the cellular AMP/ATP ratio ( 52 ). Previous studies have demonstrated that, upon energy deficiency, AMPK activation may result in increased PGC-1α expression and phosphorylation to modulate the expression of several key players in mitochondrial biogenesis and OXPHOS of fatty acids ( 53 , 54 ) ( Fig. 1 ).…”

Melanocortin 1 receptor attenuates early brain injury following subarachnoid hemorrhage by controlling mitochondrial metabolism via AMPK/SIRT1/PGC-1α pathway in rats

“…Yan et al has demonstrated that AMPK reduces ROS production through the activation of PGC-1α 21 . In addition, AMPK can indirectly activate SIRT1 by regulating the level of NAD+ 22 , which is an NAD+-dependent protein deacetylase that participates in neuroprotection by reducing oxidative stress. SIRT1 activation reportedly improves mitochondrial function and attenuates brain injury by increasing the level of PGC-1α 23 .…”

Transcriptome Analysis of Juvenile Tilapia (Oreochromis niloticus) Blood, Fed With Different Concentrations of Resveratrol

“…In cattle, the beneficial effects of dietary RES might derive in part by preventing mitochondrial ATP synthesis in tumor cells, thereby inducing apoptosis (Gledhill et al, 2007;Lin et al, 2009) via the Sirt1-PGC1α-PPARα pathway (Milton-Laskibar et al, 2018). However, it has been further confirmed in teleosts through the NAD + /NADH ratio (Zhang et al, 2017), phosphorylation (Shi et al, 2018) and acetylation (Schirmer et al, 2012) in post-transcriptional regulation levels. Though the expression of genes related with mitochondrial dysfunction and ATP synthese activity changed, future studies should be conducted to determine the actual pathways involved.…”