Browsing by Subject "lipid"
Now showing 1 - 4 of 4
Results Per Page
Sort Options
Item Algal biofuels : the effect of temperature on algal growth and lipid content(2009-08) Klenzendorf, Stephanie Marie; Marshall, Jill Ann; Mehdy, Mona Cynthia, 1955-; Sathasivan, KanagasabapathiReplacing fossil fuels with algae, a renewable resource, is an exciting possibility. This study evaluates the algae found in South Texas brackish water ponds used for aquaculture of fish as a possible source of biofuels. Samples of algae from these ponds were cultured at varying temperatures ranging from 15.5ºC to 36.5ºC. High levels of growth were observed at 20.5ºC and the highest lipid content was measured at 23.0ºC. Temperature was also a factor in the distribution of microalgal taxa throughout the temperature gradient. This information will be added to the growing body of research investigating similar cultures of algae for future biofuel production.Item Heart- and liver-type fatty acid binding proteins in lipid and glucose metabolism(Texas A&M University, 2004-11-15) Erol, ErdalHeart-type Fatty Acid-Binding Protein (H-FABP) is required for high rates of skeletal muscle long chain fatty acid (LCFA) oxidation and esterification. Here we assessed whether H-FABP affects soleus muscle glucose uptake when measured in vitro in the absence of LCFA. Wild type and H-FABP null mice were fed a standard chow or high fat diet before muscle isolation. With the chow, the mutation increased insulin-dependent deoxyglucose uptake by 141% (P<0.01) at 0.02 mU/ml of insulin, but did not cause a significant effect at 2 mU/ml insulin; skeletal muscle triglyceride and long chain acyl-CoA (LCACoA) levels remained normal. With the fat diet, the mutation increased insulin-dependent deoxyglucose uptake by 190% (P<0.01) at 2 mU/ml insulin, thus partially preventing insulin resistance, and completely prevented the threefold (P<0.001) diet-induced increase of muscle triglyceride levels; however, muscle LCACoA levels showed little or no reduction. With both diets, the mutation reduced the basal (insulinindependent) soleus muscle deoxyglucose uptake by 28% (P<0.05). These results establish a close relationship of FABP-dependent lipid pools with insulin sensitivity, and indicate the existence of a non-acute, antagonistic, and H-FABP-dependent fatty acid regulation of basal and insulin-dependent muscle glucose uptake. Liver fatty acid binding protein (L-FABP) has been proposed to limit the availability of chain LCFA for oxidation and for peroxisome proliferator-activated receptor (PPAR-alpha), a fatty acid binding transcription factor that determines the capacity of hepatic fatty acid oxidation. Here, we used L-FABP null mice to test this hypothesis. Under fasting conditions, this mutation reduced β-hydroxybutyrate (BHB) plasma levels as well as BHB release and palmitic acid oxidation by isolated hepatocytes. However, the capacity for ketogenesis was not reduced: BHB plasma levels were restored by octanoate injection; BHB production and palmitic acid oxidation were normal in liver homogenates; and hepatic expression of key PPAR-alpha target (MCAD, mitochondrial HMG CoA synthase, ACO, CYP4A3) and other (CPT1, LCAD) genes of mitochondrial and extramitochondrial LCFA oxidation and ketogenesis remained at wild-type levels. These results suggest that under fasting conditions, hepatic L-FABP contributes to hepatic LCFA oxidation and ketogenesis by a nontranscriptional mechanism.Item Lipid Metabolism in Bovine Subcutaneous Adipose Tissue of Steers Fed Supplementary Palm Oil or Soybean Oil(2012-10-19) Gang, Gyoung OkWe hypothesized that supplementing finishing diets with palm oil would elevate Stearoyl-CoA desaturase (SCD) activity in muscle and subcutaneous (s.c.) adipose tissue, promoting adipocyte differentiation and increase monounsaturated fatty acids (MUFA) in beef, particularly oleic acid. Soybean oil supplementation was used as a negative control. Eighteen Angus steers were assigned randomly to three groups of 6 steers and fed a basal diet without additional fat, with 3% palm oil (rich in palmitic acid), or with 3% soybean oil (rich in polyunsaturated fatty acids), top dressed daily. There were no significant differences across treatment in quality grade, REA, 12th rib fat thickness, or yield grade. Palm oil tended to increase marbling score (P = 0.33). Palm oil supplementation decreased the concentration of myristic acid (P = 0.04), and tended to decrease the concentration of t10, c12 CLA (P = 0.07) and 18:3n-3 (P = 0.06) in s.c. adipose tissue while soybean supplementation increased c9, t11 CLA (P = 0.02) and 18:3n-3 (P = 0.03) in muscle. Palm oil supplementation increased both glucose and acetate incorporation into total lipids of s.c. adipose tissue (both P = 0.03). Volume of s.c. adipocytes was greater in cattle supplemented with palm oil than in soybean- supplemented cattle (P = 0.004). Enzyme activity of G-6-PDH tended to be greater in steers consuming palm oil supplement (P = 0.10). We conclude that there was a partial interaction between palm oil supplementation and adipocyte differentiation. Palm oil supplementation increased s.c. adipocyte content without deteriorating meat quality traits and tended to increase marbling.Item The role of docosahexaenoic acid in mediating mitochondrial membrane lipid peroxidation and apoptosis in colonocytes.(Texas A&M University, 2005-11-01) Ng, Yee VoonColon cancer is the second leading cause of cancer death in the United States. Epidemiological data indicate that the consumption of dietary fiber and fish/marine products favorably modulate colon tumorigenesis. Docosahexaenoic acid (DHA, 22:6n-3) from fish oil, and butyrate, a fiber fermentation product generated in colon, protect against colon tumorigenesis in part by inducing apoptosis. We have shown that DHA is incorporated into mitochondrial membrane phospholipids, which enhances oxidative stress and mitochondrial membrane potential (MP) dissipation. To elucidate the subcellular origin of oxidation induced by DHA and butyrate exposure, young adult mouse colonocytes (YAMC) were treated with 0200 ??M DHA, linoleic acid (LA, 18:2n-6) or no fatty acid (control) for 72 h with or without 5 mM butyrate for the final 6-24 h. Real time analysis of cellular membrane lipid oxidation, as indicated by oxidation of a lipophilic vital dye, mitochondrial permeability transition (MPT), as characterized by MP dissipation, and cytosolic ROS production, as depicted by hydrophilic ROS reactive fluorophore accumulation, were measured by living cell fluorescence microscopy. After 24 h of butyrate treatment, DHA primed cells showed a 29% increase in lipid oxidation (p<0.01), compared to no butyrate treatment, which could be blocked by a mitochondria targeted antioxidant, MitoQ (p <0.05), whereas LA treatment did not show an effect. In the absence of butyrate, DHA treatment, compared to LA, increased resting MP by 14% (p <0.01). In addition, butyrate-induced MP dissipation was greater (20%) in DHA primed cells as compared to LA (10%). This effect was blocked by pre-incubation with MPT inhibitors, cyclosporin A or bongkrekic acid at 1 ??M. These data suggest an increase in mitochondrial lipid oxidation and the resultant change in MP may contribute to the induction of apoptosis by DHA with butyrate as shown previously.