Browsing by Subject "insulin"
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Item Effects of Maternal Nutrition Manipulation on Mares and Their Foals(2013-03-14) Winsco, Kelly NPrevious research documented the fetus is sensitive to nutrition of the dam, but this has not been thoroughly investigated in horses. Objectives of the current studies were to determine effect of manipulation of maternal nutrition during the last third of pregnancy on mare performance, intake, hormones, foaling parameters, colostrum, and foal passive transfer of immunity and growth, and effects of supplemental arginine. Plane of nutrition influenced mare performance, and DMI was influenced by time with the first trial finding all mares consumed less in the 10th month of pregnancy compared to the 11th month, and the second trial finding all mares consumed less during the 11th month. Additionally, the second study determined arginine supplementation has no detrimental effects on DMI. Both studies indicated the dual marker system was sufficient at estimating DMI. Neither trial found an influence of treatment on foaling parameters or physical measurements obtained following parturition, and the second study determined arginine supplementation also did not affect foaling or measurements. The first study determined maternal nutrition did not affect foal growth or ADG. When colostrum quality was evaluated, the first study determined mares consuming only hay had increased specific gravity and Brix% indicating higher quality. This was confirmed by IgG analysis finding a tendency for increased IgG concentration. However, colostrum volume was not affected by nutrition, nor was total g IgG. The second study found contrasting results with greater specific gravity in mares on a high plane of nutrition, and a tendency for moderate plane of nutrition mares to have greater volume. Additionally, the second study determined that arginine supplementation does not influence colostrum volume or quality (measured by specific gravity or Brix %). In the first trial, maternal diets affected glucose and insulin AUC in mares, which altered insulin dynamics in the resulting foals. Foal insulin AUC and peak insulin concentration were greater in foals from mares supplemented with concentrate compared to foals from mares fed hay alone. These studies have provided a wealth of information to help elucidate the impact of maternal nutrition in late gestation on mares and their foals.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 Influence of Maternal Plane of Nutrition and Arginine Supplementation on Mares and Their Foals: Glucose and Insulin Dynamics(2012-10-19) Hanson, AndreaThirty-two Quarter horse mares (468 to 668 kg BW; 3 to 19 yr) were utilized in a randomized complete block design. Animals were blocked by expected foaling date and randomly assigned to treatments within block. Treatments began 110 d prior to expected foaling date and were arranged as a 2 x 2 factorial consisting of two planes of nutrition, moderate (Mod; 0.5% BW as fed grain/d) or high (High; 1% BW as fed grain/d) and two levels of L-arginine supplementation, 0.21 g/kg BW/d (Arg) or no supplemental Arg (Con; L-alanine to maintain isonitrogenous diets). Mares were housed by block, allowed ad libitum access to water and coastal bermudagrass (Cynodon dactylon) hay, and fed commercial grain twice daily in individual stalls. A modified frequent sampling i.v. glucose tolerance test (FSIGT) was performed on mares during the 11th month gestation and on foals at 5 and 30 d of age. Jugular catheters were placed 1 h before FSIGT, and horses were allowed ad libitum access to bermudagrass hay and water throughout. After a baseline plasma sample was collected, a glucose bolus of 0.3 g/kg BW was administered. Blood samples were collected at 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 14, 16, and 19 min. At minute 20, an insulin bolus of 30 mU/kg BW was administered. Blood samples continued to be collected at 22, 23, 24, 25, 27, 30, 35, 40, 50, 60, 70, 80, 90, 100, 120, 150, and 180 min. Samples were placed into tubes containing sodium heparin, immediately placed on ice, and centrifuged within 20 min. Plasma was then collected, placed in microtubes and frozen at -20 degrees C for later analysis. Glucose concentrations were analyzed using a colorimetric assay and insulin concentrations determined using a commercial RIA kit. There was no influence of dietary treatment on mare glucose area under the curve (AUCg) or peak glucose (PG) and insulin (PI) concentrations (P >= 0.55). Mare insulin area under the curve (AUCi) tended to be influenced by the interaction between nutritional plane and ARG supplementation (P <= 0.06) with HighCon mares having greater AUCi than ModCon (P <= 0.05), and HighCon mares having greater AUCi than mares fed HighArg (P <= 0.05). Foal AUCg, AUCi, and PI were not influenced by maternal diet. However, PG concentration in foals tended to be influenced by mare AA supplementation with foals from Con mares having higher concentrations compared to Arg (P <= 0.09) An influence of age was observed on foal AUCg and AUCi. Foal AUCg was greater at 5 d compared to 30 d (P <= 0.003). Foal AUCi tended to be greater at 30 d compared to 5 d (P <= 0.08). Data suggest maternal plane of nutrition and arginine supplementation can alter mare and foal glucose and insulin dynamics.Item Insulin Sensitivity in Tropically Adapted Cattle With Divergent Residual Feed Intake(2012-10-19) Shafer, GentrieResidual feed intake (RFI) is one method to identify feed efficient animals; however, this method is costly and time consuming therefore, identifying an indirect measure of RFI is important. Evaluating the glucoregulatory mechanisms in cattle selected for divergent RFI may provide insight into metabolic processes involved in feed efficiency. This study evaluated the effect of a glucose (GLUC) challenge on efficient (LRFI) and inefficient (HRFI) tropically adapted bulls and heifers. Insulin (INS) secretion was determined by radioimmunoassay (RIA) and GLUC was determined by colorimetry. Insulinogenic index (IIND) was calculated as the ratio of INS to GLUC (I/G). Bonsmara heifers were evaluated in two experiments. Similar results were observed in both experiments. RFI affected (P < 0.05) INS response; with LRFI heifers having a greater INS response than HRFI heifers. Similarly, RFI affected (P < 0.05) IIND; with LRFI heifers having a greater IIND than HRFI heifers. In Santa Gertrudis bulls, RFI did not affect (P > 0.05) GLUC conc. or Ins. response; however, numerically HRFI bulls had a greater INS response than LRFI bulls. RFI affected (P < 0.05) IIND; with LRFI bulls having a lower IIND than HRFI bulls. In Brahman heifers (Exp 1), RFI did not affect (P > 0.05) GLUC concentration or INS. response; however, numerically HRFI heifers had a greater INS response than LRFI heifers. RFI affected (P < 0.05) IIND; with LRFI heifers having a lower IIND than HRFI heifers. In Brahman bulls (Exp 2), RFI affected (P > 0.05) INS response; with HRFI bulls having a greater INS response than LRFI bulls. RFI affected (P < 0.05) IIND; with LRFI bulls having a lower IIND than HRFI bulls. Bonsmara cattle evaluated for RFI had a response to an influx of exongenous glucose that was opposite to that observed in the Brahman and Santa Gertrudis cattle evaluated for RFI. Insulinogenic index was significantly different between RFI groups in each experiment. The lower amount of INS required for clearance of the GLUC from the circulation of the Brahman and Santa Gertrudis cattle fits with our hypothesis that more efficient cattle would require less INS than the less efficient cattle. Further research and studies need to establish glucoregulatory differences between breeds and sexes of cattle evaluated for RFI.Item Involvement of PFKFB3/iPFK2 in the Effects of Leucine and n-3 PUFA in Adipocytes(2012-02-14) Halim, VeraStudies had shown that leucine supplementation increases insulin sensitivity and it has been studied that n-3 PUFA may have an anti-inflammatory effect in adipocytes. However, the extent to which dietary sources such as leucine and/or n-3 PUFA act through PFKFB3/iPFK2 to suppress adipocyte inflammatory response has not been studied; PFKFB3/iPFK2 is a regulator that links adipocyte metabolism and inflammatory responses. In this study, the involvement of PFKFB3/iPFK2 in the effects of insulin sensitizing and anti-inflammatory effect of leucine and/or n-3 PUFA are explored using cultured 3T3-L1 adipocytes including wild-type cells, PFKFB3-control cells (iPFK2-Ctrl) and PFKFB3-knockdown cells (iPFK2-KD). In iPFK2-Ctrl cells, leucine supplementation appears to have insulin-sensitizing effects through improving p-Akt/Akt insulin signaling, but have no effect on adiponectin expression, and appear to have limited anti-inflammatory effects. n-3 PUFA supplementation appears to have limited effects on both insulin sensitizing and anti-inflammatory effects in iPFK2-Ctrl. In contrast, n-3 PUFA exhibit pro-inflammatory expression in iPFK2-KD. The results of this study support the hypothesis that PFKFB3/iPFK2 is critically involved in insulin-sensitizing effects of leucine. This role of PFKFB3/iPFK2, however, appears to be independent of anti-inflammatory responses. Given this, it is likely that PFKFB3/iPFK2 only account, in part, for the beneficial effects of leucine. n-3 PUFA stimulate PFKFB3/iPFK2 activity in wild-type adipocytes. However, PUFA do not exhibit anti-inflammatory and insulin-sensitizing effects in controls. In contrast, n3-PUFA exhibit proinflammatory effects in iPFK2-KD cells. Taken together, PFKFB3/iPFK2 is involved, at least in part, in the effects of insulin sensitization of leucine and appears to protect adipocytes from inflammatory responses, which could be exacerbated by n-3 PUFA when PFKFB3/iPFK2 is disrupted.