Dihydromyricetin improves liver fat deposition in high-fat diet-induced obese mice

It has been reported that the histone/protein deacetylase SIRT1-AMP-activated protein kinase(SIRT1-AMPK)signaling pathway may play a role in the effects of dihydromyricetin(DHM)on improving triglyceride(TG)accumulation and insulin resistance in liver cells.Therefore,we aimed to further observe the effect of DHM on liver fat deposition in high-fat diet(HFD)-induced obese mice and explore its possible mechanism.C57BL/6J mice were fed with a normal diet(ND)and HFD and were treated with or without low-dose(125 mg/kg)or high-dose(250 mg/kg)DHM for 16 weeks,respectively.During the experiment,body weight was checked every 2 weeks.After 16 weeks,the orbital vein was bled,the animals were sacrificed,and the subscapular,epididymal,and inguinal fat were collected and weighed with an electronic scale.An automatic biochemical analyzer was used to determine the levels of serum triglyceride(TG),serum total cholesterol(TC),serum high-density lipoprotein(HDL),and serum low-density lipoprotein(LDL).The livers were stained with hematoxylin-eosin staining(H&E)and Oil Red O to detect liver fat deposition.A colorimetric method was used to detect liver MDA and SOD contents.Quantitative real-time PCR(q RT-PCR)was used to detect the gene expressions of related indicators,such as interleukin-6(IL-6),interleukin-8(IL-8),tumor necrosis factor-α(TNF-α),acetyl-Co A carboxyl acetyl-Co A carboxylase(ACC),sterol regulatory element-binding protein-1c(SREBP-1),fatty acid synthetase(FAS),peroxisome proliferator activation receptor alpha(peroxisome proliferator-activated receptor-alpha,PPARα),palmitoyltransferase 1(carnitine palmitoyltransferase 1,CPT1),SIRT1,and AMPK.Western blotting analysis was used to detect the protein expression levels of SIRT1,AMPK,SIRT1-AMPK,ACC,SREBP-1,FAS,PPARα,and CPT1.Results showed that compared with the ND group,the weight and body fat of the mice in the HFD group were increased significantly.The levels of TG,TC,and LDL were increased,the level of HDL was decreased,the volume of hepatocytes was increased,the number of lipid droplets,fat deposition,MDA,IL-6,IL-8,TNF-α,SREBP-1c,FAS,ACC1,SIRT1,and AMPK protein levels were significantly increased,and the SOD activity,PPARα,CPT1,SIRT1 m RNA,AMPK m RNA,PPARα,CPT1 levels were significantly decreased.DHM could significantly reverse the changes of the above indexes in HFD mice,while DHM had no significant effect on the above indexes in ND mice.Collectively,our findings revealed that DHM improved liver fat deposition in HFD-induced obese mice,and the mechanism might be related to inhibition of oxidative stress,inflammation,lipid synthesis,and promotion of lipid decomposition.

Possible Role of the Submandibular Gland in the Development of Obesity in Mice

The possible role of submandiblular glands (SMG) in the development of obesity was studied in two types of genetically obese mice, ob/ob and yellow Ay: Obesity is caused by hyperplasia followed by hypertrophy in ob/ob mice and mainly by hypertrophy in Ay mice.The histological features of SMGs exhibited clear sexual dimorphism in both mice similarto lean controls. The SMGs of ob/ob mice was smaller in size and had smaller granular convoluted tubular portions than lean controls, while the SMGs of Ay mice did not differ from lean controls. Sialoadenectomy before and after development of obesity gCnerally reduced the gain of body weights in both sexes of Ay mice but not in ob/ob mice. The content of epidermal growth factor (EGF) in the SMGs was higher in Ay mice and lower in ob/ob mice than their controls. The possible role of EGF in the SMGs in the development of obesity is discussed