Effect of early high fat diet on pancreatic β cellularity and insulin sensibility in young rats
XIE Kun-Xia, XIAO Yan-Feng, XU Er-Di, YIN Chun-Yan, YI Xiao-Qing, CHANG Ming
Department of Pediatrics, Second Affiliated Hospital of Medical College, Xi'an Jiaotong Univesity, Xi'an 710004, China. Email: xiaoyanfeng0639@sina.com
Abstract OBJECTIVE: To study the effects of early high fat diet on sugar metaboliam, insulin sensibility and pancreatic β cellularity in young rats. METHODS: Sixty male weaned young rats were randomly fed with high fat diet (high fat group) and normal diet (control group). The body weight, viscus fattiness and fasting plasma glucose (FPG) were measured after 3, 6 and 9 weeks. Serum insulin level was measured with radioimmunoassay. The ultrastructure of pancreas was observed under an electricmicroscope. RESULTS: The high fat group had significantly higher body weight and visceral fat weight than the control group after 3 weeks. There were no significant differences in the FPG level between the two groups at all time points. The levels of fasting insulin and HOMAIR in the high fat group were significantly higher than those in the control group after 3, 6 and 9 weeks (P<0.01). Dilation of rough endoplasmic reticulum and mild swelling of mitochondria of islet β-cells were observed in the high fat group after 6 weeks. CONCLUSIONS: Early high fat diet may induce a reduction in insulin sensitivity and produce insulin resistance in young rats. Endoplasmic reticulum expansion in β-cells may be an early sign of β-cell damage due to obesity.[Chin J Contemp Pediatr, 2010, 12 (9):740-743]
XIE Kun-Xia,XIAO Yan-Feng,XU Er-Di et al. Effect of early high fat diet on pancreatic β cellularity and insulin sensibility in young rats[J]. 中国当代儿科杂志, 2010, 12(09): 740-743.
XIE Kun-Xia,XIAO Yan-Feng,XU Er-Di et al. Effect of early high fat diet on pancreatic β cellularity and insulin sensibility in young rats[J]. CJCP, 2010, 12(09): 740-743.
[1]Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity[J]. N Eng1 J Med, 2002, 364 (11): 802-810.
[2]Caceres M, Teran CG, Rodriguez S, Medina M. Prevalence of insulin resistance and its association with metabolic syndrome criteria among Bolivian children and adolescents with obesity[J]. BMC Pediatrics, 2008, 8(12):31-36.
[4]Miyazaki Y, Glass L, Triplitt C, Wajcberg E, Mandarino LJ, DeFronzo RA. Abdominal fat distribution and peripheral and inshlin resistance in type 2 diabets mellitus[J]. Pediatr Endocrinol Metab, 2002, 283(6):1135-1143.
[5]Pietil-inen KH, Rissanen A, Kaprio J, M-kimattila S, H-kkinen AM, Westerbacka J, et al. Acquired obesity is associated with increased liver fat, intra-abdominal fat, and insulin resistance in young adult monozygotic twins[J]. Am J Physiol Endocrinol Metab, 2005, 288(4):E768-774.
[7]Hayashi T, Boyko EJ, Leonetti DL, McNeely MJ, Newell-Morris L, Kahn SE, et al . Visceral adiposity and the risk of impaired glucose tolerance: a prospective study among Japanese Americans[J]. Diabetes Care, 2003, 26 (3):650-655.
[8]Steppan CM, Lazar MA. Resistin and obesity-associated insulin resistance[J]. Trends Endocrinol Metab, 2002, 13(1): 18-23.
[10]Matveyenko AV, Butler PC. Beta-cell deficit due to increased apoptosis in the human islet amyloid polypeptide transgenic (HIP) rat recapitulates the metabolic defects present in type 2 diabetes[J]. Diabetes, 2006, 55(7):2106-2114.
[11]Thomas HE, McKenzie MD, Angstetra E, Campbell PD, Kay TW. Beta cell apoptosis in diabetes[J]. Apoptosis, 2009, 14(12):1389-1404.
[12]Piro S, Anello M, Di Pietro C, Lizzio MN, Patanè G, Rabuazzo AM, et al. Chronice exposure to free fatty acid or high glucose induces apoptosis in rat pancreaticislets: possible role of oxidative stress[J]. Metabolism, 2002, 51(10):1340-1347.
[13]Eizirik DL, Cardozo AK, Cnop M. The role for endoplasmic reticulum stress in diabetes mellitus[J]. Endocr Rev, 2008, 29(1):42-61.
[14]Scheuner D, Kaufman RJ. The unfolded protein response:a pathway that links insulin demand with beta-cell failure and diabetes[J]. Endocr Rev, 2008, 29(3):317-333.
[15]Haynes CM, Titus EA, Cooper AA. Degradation of misfolded proteins prevents ER-derived oxidative stress and cell death[J]. Mol Cell, 2004, 15(5): 767-776.