Journal
CURRENT DIABETES REPORTS
Volume 9, Issue 1, Pages 43-50Publisher
CURRENT MEDICINE GROUP
DOI: 10.1007/s11892-009-0009-6
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Funding
- NCRR NIH HHS [M01 RR 00034, M01 RR000109, M01 RR000073, M01 RR 00073, M01 RR000034, M01 RR00109] Funding Source: Medline
- NIDDK NIH HHS [R01 DK55384, R01 DK073284-02, R01 DK055384-05, R01 DK073284, R01 DK055384] Funding Source: Medline
- PHS HHS [R01 073284] Funding Source: Medline
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In humans, insulin sensitivity is relatively impaired by diets that are low in oleic acid (OA), a cis monounsaturated fatty acid (MUFA), or rich in trans MUFA or palmitic acid (PA), a saturated fatty acid (FA). Emerging evidence exists that PA, in contrast to OA, causes insulin resistance via stimulation of inflammatory signaling and production of cytosolic lipid compounds (diacylglycerol and ceramide), leading one to presume that dietary or pharmacologic maneuvers that facilitate transport of FA into the mitochondria would be beneficial. However, in some models, insulin resistance is caused by excessive FA transport into the mitochondria, coupled with deficient electron transport and possibly increased reactive oxygen species formation; PA may impair electron transport via effects on gene expression. A research challenge is to determine whether feeding humans diets with markedly different contents of PA and OA would alter insulin sensitivity and/or critical biochemical mechanisms impacting muscle insulin signaling.
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