| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Medicine, University Of Pittsburgh, Pittsburgh, Pennsylvania, United States
2 Medicine of Endocrinology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States; Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, Pennsylvania, 15261, United States
* To whom correspondence should be addressed. E-mail: huangw{at}dom.pitt.edu.
High sucrose (HS) feeding induces hepatic steatosis and plasma dyslipidemia. In previous reports we demonstrated a rapid leptin-induced decrease in liver and plasma VLDL triglycerides (TG) in lean rats, effects that were abolished in obese rats fed a high fat diet, a model that also presents with hepatic steatosis/plasma dyslipidemia. To further examine the capacity of acute leptin treatment to improve metabolic abnormalities induced by nutrient excess, hepatic leptin action was studied in rats after 5 weeks of HS feeding. HS induced hepatic steatosis (TG +80±8%, P=0.001), plasma hyperlipidemia (VLDL-TG +102±14%, P=0.001), hyperinsulinemia (plasma insulin +67±12%, P=0.04), and insulin resistance as measured by HOMA (+125±20%, P=0.02), without increases in adiposity or plasma leptin concentration when compared to standard chow (SC) fed controls. A 120-min leptin infusion (plasma leptin 13.6±0.7 ng/ml) in HS corrected hepatic steatosis (LTG -29±3%, P=0.003) and plasma hyperlipidemia (VLDL-TG -42±4%, P=0.001) and increased plasma ketones (+45±3%, P=0.006), without altering plasma glucose, insulin or HOMA compared to saline-infused HS controls. Additionally, leptin activated liver PI3-kinase (+70±18%, P=0.01) and Akt (+90±29%, P=0.02), and inhibited ACC (40±7%, P=0.04) in HS, further demonstrating that hepatic leptin action was intact in HS. We conclude that (1) leptin action on hepatic lipid metabolism remains intact in HS rats; (2) leptin rapidly reverses hepatic steatosis and plasma dyslipidemia induced by sucrose, and (3) the preservation of hepatic leptin action after a high sucrose diet is associated with the maintenance of low adiposity and plasma leptin concentrations.
This article has been cited by other articles:
|
|
 |
|
  T. Uebanso, Y. Taketani, M. Fukaya, K. Sato, Y. Takei, T. Sato, N. Sawada, K. Amo, N. Harada, H. Arai, et al. Hypocaloric high-protein diet improves fatty liver and hypertriglyceridemia in sucrose-fed obese rats via two pathways Am J Physiol Endocrinol Metab, July 1, 2009; 297(1): E76 - E84. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Huang, A. Metlakunta, N. Dedousis, H. K. Ortmeyer, M. Stefanovic-Racic, and R. M. O'Doherty Leptin Augments the Acute Suppressive Effects of Insulin on Hepatic Very Low-Density Lipoprotein Production in Rats Endocrinology, May 1, 2009; 150(5): 2169 - 2174. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. J. Vieira, R. J. Valentine, K. R. Wilund, N. Antao, T. Baynard, and J. A. Woods Effects of exercise and low-fat diet on adipose tissue inflammation and metabolic complications in obese mice Am J Physiol Endocrinol Metab, May 1, 2009; 296(5): E1164 - E1171. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
