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osu1180477953.pdf (8.46 MB)
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Mechanisms of conjugated linoleic acid on insulin resistance, hepatic steatosis, and adiposity
Author Info
Wendel, Angela A
Permalink:
http://rave.ohiolink.edu/etdc/view?acc_num=osu1180477953
Abstract Details
Year and Degree
2007, Doctor of Philosophy, Ohio State University, Ohio State University Nutrition.
Abstract
Conjugated linoleic acid (CLA), a group of dietary fatty acids, decreases body weight primarily through the reduction of adipose mass and is reported to modulate insulin resistance. The mechanisms by which CLA depletes adipose and the roles of adipokines in CLA-mediated insulin resistance are not completely understood. The first objective of this research was to determine the effects of CLA on lipid metabolism and fatty acid composition in the livers of Zucker diabetic fatty (fa/fa; ZDF) rats compared to a thiazolidinedione (TZD). CLA reduced adipose mass while improving glucose tolerance and hepatic steatosis in ZDF rats. The effects of CLA and TZD on hepatic lipid composition suggest that the effects of these two agents on glucose tolerance may be associated with a reduction in stearoyl-CoA desaturase-1. In mice, CLA rapidly reduces adipose mass and worsens insulin resistance and hepatic steatosis, effects which are preceded by the significant depletion of the adipokines leptin and adiponectin. Therefore, the second objective was to determine whether effects of CLA on insulin resistance, hepatic steatosis, and inflammation depend on the depletion of leptin by CLA. Recombinant leptin was co-administered with dietary CLA in ob/ob mice to, in effect, negate the leptin depletion effect of CLA. In both the absence and presence of leptin, CLA significantly reduced adipose mass and depleted adiponectin. In the absence of leptin, CLA worsened insulin resistance without evidence of inflammation in adipose tissue or hepatic steatosis. In the presence of leptin, CLA failed to worsen insulin resistance, but induced hyperinsulinemia and hepatic steatosis in ob/ob mice. The significant depletion of adipose in mice by CLA may contribute to the lipodystrophic-like effects that accompany. The final objective of this research was to determine mechanisms by which CLA reduces adipose mass. The depletion of adipose tissue in ob/ob mice by CLA was accompanied by the acquirement of brown adipose-like characteristics, such as increased CPT-1b, PGC-1α, and UCP-1, in the white adipose of CLA-fed mice. This alteration may facilitate the reduction of adipose mass by increasing mitochondrial oxidation and energy dissipation. However, it appears that CLA does not increase UCP-1 through β3AR signaling.
Committee
Martha Belury (Advisor)
Pages
216 p.
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Citations
Wendel, A. A. (2007).
Mechanisms of conjugated linoleic acid on insulin resistance, hepatic steatosis, and adiposity
[Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1180477953
APA Style (7th edition)
Wendel, Angela.
Mechanisms of conjugated linoleic acid on insulin resistance, hepatic steatosis, and adiposity.
2007. Ohio State University, Doctoral dissertation.
OhioLINK Electronic Theses and Dissertations Center
, http://rave.ohiolink.edu/etdc/view?acc_num=osu1180477953.
MLA Style (8th edition)
Wendel, Angela. "Mechanisms of conjugated linoleic acid on insulin resistance, hepatic steatosis, and adiposity." Doctoral dissertation, Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1180477953
Chicago Manual of Style (17th edition)
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Document number:
osu1180477953
Download Count:
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Copyright Info
© 2007, all rights reserved.
This open access ETD is published by The Ohio State University and OhioLINK.