2011 ADA Posters 1261-2041.indd - Diabetes

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1839-P Omega-3 Fatty Acids Protect Against Glucose Intolerance and Attenuate Ceramide Accumulation with High Fat Diet IAN LANZA, AGNIESZKA ZABIELSKI, PIOTR ZABIELSKI, DANIEL JAKAITIS, BUSHRA ALI, K. SREEKUMARAN NAIR, Rochester, MN Lipotoxicity is implicated as a cause of insulin resistance. Accumulation of lipid metabolites (e.g., ceramides) may interfere with insulin signaling in muscle. Dietary omega-3 fatty acids (n3PUFA) are reported to protect against insulin resistance with high-fat diets. We determined the impact of n3PUFA on the content and composition of lipid metabolites in skeletal muscle. Mice were fed for 10wks with normal fat diet (NF, 10% fat), high fat diet (HF, 60% fat), or high fat diet + fi sh oil (HF+N3, 60% fat with 3.4% kcals from n3PUFA). Oral glucose tolerance tests (OGTT) were performed at baseline and 10wks. Muscle tissue was homogenized and separated into sarcoplasmic, myofi brillar, and mitochondrial fractions. Ceramides and long chain acyl coA (LCACoA) were measured by mass spectrometry using internal standards for individual species. OGTT revealed signifi cant reductions in glucose tolerance in HF but not HF+N3 or NFD. Total ceramide was increased in HF (15.69±0.41 ng/ mg tissue) and HF+N3 (14.38±0.16) compared to NFD (13.05±0.43). Closer examination of individual ceramide species revealed that n3-PUFAs completely prevented HF-induced increases in medium chain saturated (C18) ceramides (NF: 7.38±0.31, HF: 9.41±0.27, HF+N3: 8.08±0.17 ng/mg tissue), but signifi cantly increased levels of long chain monounsaturated (C24:1) ceramides ceramides (NF: 2.74±0.06, HF: 2.45±0.06, HF+N3: 2.76±0.04 ng/mg tissue). Regression analyses revealed that C18 ceramide content is a strong predictor (R 2 =0.57, P
Integrated Physiology/ Obesity POSTERS 1843-P Pyruvate Dehydrogenase Kinase 2 (PDK2) Defi ciency Reduces Fasting Blood Glucose Levels and Fat Accumulation in the Liver of Mice Fed a High Fat Diet YOUNGHOON GO, NAM HO JEOUNG, JIYUN JEONG, HYEON-JI KANG, KEUN- GYU PARK, EON-JU JEON, CHANG JOO OH, AE-KYUNG MIN, JEONG-KOOK KIM, SUN JOO LEE, HYUN-AE SEO, ROBERT A. HARRIS, IN-KYU LEE, Daegu, Republic of Korea, Indianapolis, IN Regulation of the activity of the pyruvate dehydrogenase complex (PDC) is critical for disposal of excess glucose, fuel selection by tissues, and conservation of substrates for glucose synthesis. A dominant role for PDK4 in down regulation of PDC activity is suggested by the remarkable up regulation of PDK4 during fasting. This hypothesis is supported by reduced fasting levels of blood glucose levels and three carbon gluconeogenic substrates in PDK4 knockout (PDK4 -/- ) mice. Relative to PDK4, less evidence has existed for an important role for PDK2 in glucose homeostasis. Although ubiquitously expressed, PDK2 is only modestly increased by fasting, and PDK2 defi ciency has no effect upon fasting blood glucose levels in chow fed mice. However, in studies with mice fed a high fat diet for 16 weeks (12-13 mice per group), PDK2 defi ciency reduced body weight (WT vs PDK2 -/- , 49.8±0.8 vs 42.8±1.2 g, Mean±SE, P
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2011 ADA Posters 1261-2041.indd - Diabetes

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