Electronic Thesis and Dissertation Repository


Master of Science


Physiology and Pharmacology


Dr. Timothy RH Regnault


Low birth weight offspring are at increased risk for developing metabolic syndrome in later life, specifically its precursor, insulin resistance (IR). Reduced mitochondrial lipid metabolism is implicated in IR pathogenesis, promoting accumulation of acylcarnitines, and potentiating alterations in phosphorylation status of insulin signaling intermediates. While high-energy Western diets are classically implicated in IR progression, the in utero environment was recently highlighted as a major programming mechanism of later life IR. Using a guinea pig model of placental insufficiency, we investigated how an adverse in utero environment impacts later life mitochondrial lipid metabolism and IR progression, as well as its interaction with a postnatal Western diet. Markers of mitochondrial dysfunction and reduced lipid metabolism, including acylcarnitine accumulation, were observed in conjunction with disrupted phosphorylation of insulin signaling intermediates in skeletal muscle of low birth weight offspring. Additionally, a postnatal Western diet unmasked low birth weight-induced mitochondrial dysfunctions, promoting further acylcarnitine accumulation.

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