title: Eriobotrya japonica improves hyperlipidemia and reverses insulin resistance in high-fat-fed mice.
abstract: The effect of Eriobotrya japonica Lindl. (loquat) on insulin resistance was examined in mice fed a high-fat (HF) diet. First, the mice were divided randomly into two groups: the control (CON) group was fed a low-fat diet, whereas the experimental group was fed with a 45% HF diet for 10 weeks. After 6 weeks of induction, the HF group was subdivided into five groups and was given orally loquat or not for 4 weeks afterward. It was demonstrated that loquat was effective in ameliorating the HF diet-induced hyperglycemia, hyperleptinemia, hyperinsulinemia and hypertriglyceridemia, as well as in decreasing the levels of free fatty acid (FFA), but increasing the adipose PPARγ (peroxisomal proliferator-activated receptor γ) and hepatic PPARα mRNA levels. Loquat significantly decreased the body weight gain, weights of white adipose tissue and visceral fat accompanying the suppressed leptin mRNA levels. Loquat not only suppressed the hepatic mRNA levels of enzymes involved in fatty acid and triacylglycerol synthesis and lowered the sterol regulatory element binding protein-1c (SREBP-1c) mRNA level, but also affected fatty acid oxidation enzyme levels. These regulations may contribute to triacylglycerol accumulation in white adipose tissue. The findings provide a nutritional basis for the use of loquat as a functional food factor that may have benefits for the prevention of hyperlipidemia and diabetes.
authors.affiliation: Institute of Pharmaceutical Science and Technology, College of Health Science, Central Taiwan University of Science and Technology, No. 666, Buzih Road, Beitun Road, Beitun District, Taichung City 40601, Taiwan, ROC. ccshih@ctust.edu.tw
authors.forename: Chun-Ching
authors.initials: CC
authors.lastname: Shih
authors.forename: Cheng-Hsiu
authors.initials: CH
authors.lastname: Lin
authors.forename: Jin-Bin
authors.initials: JB
authors.lastname: Wu
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D054392:Adipokines / Q000032:analysis; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000284:Administration, Oral; D000818:Animals; D031983:Eriobotrya / Q000737:chemistry*; D005230:Fatty Acids, Nonesterified / Q000032:analysis; D005951:Glucose Tolerance Test; D006946:Hyperinsulinism / Q000188:drug therapy; D006949:Hyperlipidemias / Q000188:drug therapy*; D015228:Hypertriglyceridemia / Q000188:drug therapy; D007333:Insulin Resistance; D020738:Leptin / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D047495:PPAR gamma / Q000032:analysis; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000378:metabolism; D015430:Weight Gain / Q000187:drug effects
chemical_list: D054392:Adipokines; D005230:Fatty Acids, Nonesterified; D020738:Leptin; D047495:PPAR gamma; D010936:Plant Extracts; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1; D055372:AMP-Activated Protein Kinases