Sodium Acetate Stimulates The Fat Deposition By Stimulating The Fish Food Intake And The Secretion Of Insulin

Short-chain fatty acids(SCFAs)are produced by intestinal microbial fermentation of non-digestible carbohydrates and they are organic acids with 1 to 6 carbon atoms,including acetate,propionate,butyrate,etc.With the development of intestinal microbiology,microbial metabolites-SCFAs,have been reported to have important physiological functions.In mammals,acetate has been reported to regulate host body weight,glucose balance,and insulin sensitivity.However,in aquatic animals,acetate mechanism is rarely reported.In the first part of this study,we investigated the role of acetate on aquatic animals using a zebrafish(Danio rerio)model,We feed the zebrafish as satisfaction feeding method.The diets were added different concentrations of sodium acetate(0.05%,0.1%,0.15%,0.2%),The duration of the study was 2 weeks,and the results showed that 0.15% sodium acetate addition significantly increased zebrafish weight gain(P<0.05)and daily food intake(P<0.05).Detection of zebrafish feeding metabolic energy,standard metabolic energy(RS),and active metabolic energy(Ra)found that 0.15% treatment group’s decreased(P<0.05)and sodium acetate increased zebrafish energy conversion efficiency(P<0.01),indicating that sodium acetate promotes zebrafish energy accumulation.Next,we examined zebrafish body composition,liver triglyceride content(TG),hepatic oil red staining,hepatic HE slices,and muscle HE slice,our results showed that the diet add sodium acetate can promote zebrafish liver’s fat deposition.The influence of sodium acetate on the gene expression level of glucose metabolism,lipid metabolism and protein metabolism in zebrafish was determined,The results showed that the glycolytic gene expression level of zebrafish intestine decreased significantly(P<0.05),the intestinal protein synthesis gene was significantly increased,and the protein degradation gene was significantly reduced(P<0.05).The level of liver fat synthesis gene expression,protein synthesis and degrading gene expression level increased significantly(P<0.05),indicating that sodium acetate promoted zebrafish fat and protein synthesis,and inhibited zebrafish’s glycolysis and protein degradation.The blood glucose level of zebrafish 4h-6h after meal was also measured,and we found that the blood glucose level in the sodium acetate group was significantly lower(P<0.05),indicating that the addition of sodium acetate promotes the secretion of insulin.On the other hand,the expression level of orexigenic and anorexigenic genes in the brain was determinated,the results showed that 0.15% treatment group significantly increased the level of expression of the orexigenic genes(P < 0.05).In the second part of the experiment was to exclude the effect of excessive intake of sodium acetate on zebrafish growth.Feeding zebrafish with limiting 0.15% sodium acetate diet significantly increased the weight gain(P<0.05)and feed conversion efficiency(P<0.05)of zebrafish,and promote the accumulation of dirty fat in zebrafish liver.In the third part of this study,a model of zebrafish ventricle injection was established to further explore the mechanism of sodium acetate.Sodium acetate was injected into the ventricles of the adult zebra fish.The total intake of food was collected by the statistics of 2 h,4 h,6 h,8 h,24 h and 48 h,Cumulative food intake was significantly increased by ICV administration of sodium acetate(at 1.2 μmol/g body weight,BW)during a 48 h observation period after treatment.At the same time,the change of feeding gene expression was detected at different time points after ICV administration.It was found that sodium acetate could improve the expression of feeding gene.Similarly,the levels of blood glucose and insulin after zebrafish intracerebral injection at 2 h,4 h and 6 h and the gene of insulin secretion in brain,hepatic,intestinal at different time points were determined,The results showed that sodium acetate injection significantly increased the gene expression of insulin secretion and plasma insulin level.In the fourth part of this study,to further explore the pathway of sodium acetate in the brain circulation,a model of CO-injection of sodium acetate and atropine in zebrafish ventricle was established.The zebrafish ventricles co injected(1)saline;(2)atropine + saline;(3)atropine + sodium acetate 1.2 umol/g BW;(4)saline + sodium acetate 1.2 umol/gBW.On the one hand,the changes of blood glucose and insulin levels after zebrafish intracerebral injection at 2 h,4 h and 6 h were measured.On the other hand,the levels of orexigenic and anorexigenic and the brain,hepatic,intestine tissues’ s insulin secretion gene expression were detected,Our findings suggest that a co injection of atropine in the ventricles can prevent the effect of sodium acetate.Atropine,as a parasympathetic nerve inhibitor,indicates that sodium acetate plays a role through the parasympathetic nerve.The study found that sodium acetate promotes weight gain in zebrafish mainly because sodium acetate participates in the cerebral circulation through the parasympathetic system to increase the expression level of feeding genes and increase the level of zebrafish insulin,making the zebrafish in the sodium acetate treatment group more susceptible to hunger.This led to zebrafish feeding intake and liver TAG levels increased,which ultimately led to weight gain and fat accumulation.