title: Trehalose prevents adipocyte hypertrophy and mitigates insulin resistance.
abstract: Trehalose has been shown to evoke lower insulin secretion than glucose in oral saccharide tolerance tests in humans. Given this hypoinsulinemic effect of trehalose, we hypothesized that trehalose suppresses adipocyte hypertrophy by reducing storage of triglyceride and mitigates insulin resistance in mice fed a high-fat diet (HFD). Mice were fed an HFD and given drinking water containing 2.5% saccharide (glucose [Glc], trehalose [Tre], maltose [Mal], high-fructose corn syrup, or fructose [Fru]) ad libitum. After 7 weeks of HFD and saccharide intake, fasting serum insulin levels in the Tre/HFD group were significantly lower than in the Mal/HFD and Glc/HFD groups (P < .05). Furthermore, the Tre/HFD group showed a significantly suppressed elevation of homeostasis model assessment-insulin resistance compared with the Mal/HFD group (P < .05) and showed a trend toward lower homeostasis model assessment-insulin resistance than the Glc/HFD group. After 8 weeks of feeding, mesenteric adipocyte size in the Tre/HFD group showed significantly less hypertrophy than the Glc/HFD, Mal/HFD, high-fructose corn syrup/HFD, or Fru/HFD group. Analysis of gene expression in mesenteric adipocytes showed that no statistically significant difference in the expression of monocyte chemoattractant protein-1 (MCP-1) messenger RNA (mRNA) was observed between the Tre/HFD group and the distilled water/standard diet group, whereas a significant increase in the MCP-1 mRNA expression was observed in the Glc/HFD, Mal/HFD, Fru/HFD, and distilled water/HFD groups. Thus, our data indicate that trehalose prevents adipocyte hypertrophy and mitigates insulin resistance in HFD-fed mice by reducing insulin secretion and down-regulating mRNA expression of MCP-1. These findings further suggest that trehalose is a functional saccharide that mitigates insulin resistance.
authors.affiliation: Biomedical Institute, Research Center, Hayashibara Biochemical Laboratories, Inc., 675-1 Fujisaki, Okayama 702-8006, Japan. fujisaki@hayashibara.co.jp
authors.forename: Chikako
authors.initials: C
authors.lastname: Arai
authors.forename: Norie
authors.initials: N
authors.lastname: Arai
authors.forename: Akiko
authors.initials: A
authors.lastname: Mizote
authors.forename: Keizo
authors.initials: K
authors.lastname: Kohno
authors.forename: Kanso
authors.initials: K
authors.lastname: Iwaki
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Hanaya
authors.forename: Shigeyuki
authors.initials: S
authors.lastname: Arai
authors.forename: Simpei
authors.initials: S
authors.lastname: Ushio
authors.forename: Shigeharu
authors.initials: S
authors.lastname: Fukuda
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000473:pathology; D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D004041:Dietary Fats / Q000009:adverse effects; D019422:Dietary Sucrose / Q000008:administration & dosage*; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006984:Hypertrophy; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D012333:RNA, Messenger / Q000378:metabolism; D014199:Trehalose / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D018932:Chemokine CCL2; D004041:Dietary Fats; D019422:Dietary Sucrose; D007328:Insulin; D012333:RNA, Messenger; D014199:Trehalose