883 research outputs found

    Small Litter Sizes and Relative Clutch Mass of Northern Watersnakes (Nerodia sipedon sipedon) in Southwestern Ohio

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    Author Institution: Dept of Zoology, Miami UniversityRelative clutch mass (RCM), the ratio of total mass of a clutch to the postpartum body mass of the female, is considered by many a life history trait that indirectly quantifies reproductive effort in snakes. e Northern Watersnake (Nerodia sipedon sipedon) is one of the most abundant and widespread species of snake within Ohio. Litter sizes of N. s. sipedon have been reported to range between four and 99 and RCM values typically fall between 0.20 and 0.38. Two gravid N. s. sipedon were hand collected from Collins Creek (Butler County, Ohio) and maintained in the laboratory until parturition. Females gave birth to three and six neonates with RCM values of 0.108 and 0.120, respectively. The extremely small litter sizes and RCM values are, by far, the lowest ever recorded for this species in Ohio and throughout their entire North American range. This local population should be investigated further to determine if and how reproductive output is being depressed at Collins Creek

    Transcriptomic characterization of two major Fusarium resistance quantitative trait loci (QTLs), Fhb1 and Qfhs.ifa-5A, identifies novel candidate genes

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    Fusarium head blight, caused by Fusarium graminearum, is a devastating disease of wheat. We developed near-isogenic lines (NILs) differing in the two strongest known F. graminearum resistance quantitative trait loci (QTLs), Qfhs.ndsu-3BS (also known as resistance gene Fhb1) and Qfhs.ifa-5A, which are located on the short arm of chromosome 3B and on chromosome 5A, respectively. These NILs showing different levels of resistance were used to identify transcripts that are changed significantly in a QTL-specific manner in response to the pathogen and between mock-inoculated samples. After inoculation with F. graminearum spores, 16 transcripts showed a significantly different response for Fhb1 and 352 for Qfhs.ifa-5A. Notably, we identified a lipid transfer protein which is constitutively at least 50-fold more abundant in plants carrying the resistant allele of Qfhs.ifa-5A. In addition to this candidate gene associated with Qfhs.ifa-5A, we identified a uridine diphosphate (UDP)-glycosyltransferase gene, designated TaUGT12887, exhibiting a positive difference in response to the pathogen in lines harbouring both QTLs relative to lines carrying only the Qfhs.ifa-5A resistance allele, suggesting Fhb1 dependence of this transcript. Yet, this dependence was observed only in the NIL with already higher basal resistance. The complete cDNA of TaUGT12887 was reconstituted from available wheat genomic sequences, and a synthetic recoded gene was expressed in a toxin-sensitive strain of Saccharomyces cerevisiae. This gene conferred deoxynivalenol resistance, albeit much weaker than that observed with the previously characterized barley HvUGT13248

    Regulation of Exogenous and Endogenous Glucose Metabolism by Insulin and Acetoacetate in the Isolated Working Rat Heart A Three Tracer Study of Glycolysis, Glycogen Metabolism, and Glucose Oxidation

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    Abstract Myocardial glucose use is regulated by competing substrates and hormonal influences. However, the interactions of these effectors on the metabolism of exogenous glucose and glucose derived from endogenous glycogen are not completely understood. In order to determine changes in exogenous glucose uptake, glucose oxidation, and glycogen enrichment, hearts were perfused with glucose (5 mM) either alone, or glucose plus insulin (40 U/ml), glucose plus acetoacetate (5 mM), or glucose plus insulin and acetoacetate, using a three tracer ( 3 H, 14 C, and 13 C) technique. Insulinstimulated glucose uptake and lactate production in the absence of acetoacetate, while acetoacetate inhibited the uptake of glucose and the oxidation of both exogenous glucose and endogenous carbohydrate. Depending on the metabolic conditions, the contribution of glycogen to carbohydrate metabolism varied from 20-60%. The addition of acetoacetate or insulin increased the incorporation of exogenous glucose into glycogen twofold, and the combination of the two had additive effects on the incorporation of glucose into glycogen. In contrast, the glycogen content was similar for the three groups. The increased incorporation of glucose in glycogen without a significant change in the glycogen content in hearts perfused with glucose, acetoacetate, and insulin suggests increased glycogen turnover. We conclude that insulin and acetoacetate regulate the incorporation of glucose into glycogen as well as the relative contributions of exogenous glucose and endogenous carbohydrate to myocardial energy metabolism by different mechanisms. ( J. Clin. Invest. 1997. 100:2892-2899.) Key words: citric acid cycle • NMR • isotopomer analysi

    Alterations in Postprandial Hepatic Glycogen Metabolism in Type 2 Diabetes

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    Decreased skeletal muscle glucose disposal and increased endogenous glucose production (EGP) contribute to postprandial hyperglycemia in type 2 diabetes, but the contribution of hepatic glycogen metabolism remains uncertain. Hepatic glycogen metabolism and EGP were monitored in type 2 diabetic patients and nondiabetic volunteer control subjects (CON) after mixed meal ingestion and during hyperglycemic-hyperinsulinemic-somatostatin clamps applying 13C nuclear magnetic resonance spectroscopy (NMRS) and variable infusion dual-tracer technique. Hepatocellular lipid (HCL) content was quantified by 1H NMRS. Before dinner, hepatic glycogen was lower in type 2 diabetic patients (227 ± 6 vs. CON: 275 ± 10 mmol/l liver, P < 0.001). After meal ingestion, net synthetic rates were 0.76 ± 0.16 (type 2 diabetic patients) and 1.36 ± 0.15 mg · kg−1 · min−1 (CON, P < 0.02), resulting in peak concentrations of 283 ± 15 and 360 ± 11 mmol/l liver. Postprandial rates of EGP were ∼0.3 mg · kg−1 · min−1 (30–170 min; P < 0.05 vs. CON) higher in type 2 diabetic patients. Under clamp conditions, type 2 diabetic patients featured ∼54% lower (P < 0.03) net hepatic glycogen synthesis and ∼0.5 mg · kg−1 · min−1 higher (P < 0.02) EGP. Hepatic glucose storage negatively correlated with HCL content (R = −0.602, P < 0.05). Type 2 diabetic patients exhibit 1) reduction of postprandial hepatic glycogen synthesis, 2) temporarily impaired suppression of EGP, and 3) no normalization of these defects by controlled hyperglycemic hyperinsulinemia. Thus, impaired insulin sensitivity and/or chronic glucolipotoxicity in addition to the effects of an altered insulin-to-glucagon ratio or increased free fatty acids accounts for defective hepatic glycogen metabolism in type 2 diabetic patients

    First Trimester Plasma Glucose Values in Women without Diabetes are Associated with Risk for Congenital Heart Disease in Offspring

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    In a retrospective study of 19 171 mother-child dyads, elevated random plasma glucose values during early pregnancy were directly correlated with increased risk for congenital heart disease in offspring. Plasma glucose levels proximal to the period of cardiac development may represent a modifiable risk factor for congenital heart disease in expectant mothers without diabetes.Peer reviewe

    Reversal of Hypertriglyceridemia, Fatty Liver Disease, and Insulin Resistance by a Liver-Targeted Mitochondrial Uncoupler

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    SummaryNonalcoholic fatty liver disease (NAFLD) affects one in three Americans and is a major predisposing condition for the metabolic syndrome and type 2 diabetes (T2D). We examined whether a functionally liver-targeted derivative of 2,4-dinitrophenol (DNP), DNP-methyl ether (DNPME), could safely decrease hypertriglyceridemia, NAFLD, and insulin resistance without systemic toxicities. Treatment with DNPME reversed hypertriglyceridemia, fatty liver, and whole-body insulin resistance in high-fat-fed rats and decreased hyperglycemia in a rat model of T2D with a wide therapeutic index. The reversal of liver and muscle insulin resistance was associated with reductions in tissue diacylglycerol content and reductions in protein kinase C epsilon (PKCε) and PKCθ activity in liver and muscle, respectively. These results demonstrate that the beneficial effects of DNP on hypertriglyceridemia, fatty liver, and insulin resistance can be dissociated from systemic toxicities and suggest the potential utility of liver-targeted mitochondrial uncoupling agents for the treatment of hypertriglyceridemia, NAFLD, metabolic syndrome, and T2D

    1972 Research Progress Reports, Fruit and Vegetable Processing and Food Technology

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    Evaluation of tomato cultivars / W. A. Gould, James Black, Louise Howiler, Shirley Perryman, and Stanley Z. Berry -- Effects of food additives on the quality of canned tomatoes / Wilbur A. Gould, John Mount, Jacquelyn Gould, Louise Howiler, and James Black -- Effect of storage temperature on shelf life of ascorbic acid fortified tomato juice / Gerald A. Pope and Wilbur A. Gould -- Survey of waste disposal practices of Ohio tomato processors / J. R. Geisman -- Evaluation of snap bean varieties for processing / Wilbur A. Gould, Jacquelyn Gould and Roberta Topits -- The effect of variety, size, and fermentation temperature on the quality attributes of cucumber pickles / Gary Flinn and Wilbur A. Gould -- Progress report on frozen corn-on-the-cob / James W. Swinehart and Wilbur A. Gould -- Progress report on cabbage lipids / Andrew C. Peng -- Effect of soybean flour on quality and protein content in the manufacture of doughnuts / Mohamed I. Mahmoud and Wilbur A. Goul

    Membrane-Bound sn-1,2-Diacylglycerols Explain the Dissociation of Hepatic Insulin Resistance from Hepatic Steatosis in MTTP Knockout Mice

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    Microsomal triglyceride transfer protein (MTTP) deficiency results in a syndrome of hypolipidemia and accelerated NAFLD. Animal models of decreased hepatic MTTP activity have revealed an unexplained dissociation between hepatic steatosis and hepatic insulin resistance. Here, we performed comprehensive metabolic phenotyping of liver-specific MTTP knockout (L-Mttp(-/-)) mice and age-weight matched wild-type control mice. Young (10-12-week-old) L-Mttp(-/-) mice exhibited hepatic steatosis and increased DAG content; however, the increase in hepatic DAG content was partitioned to the lipid droplet and was not increased in the plasma membrane. Young L-Mttp(-/-) mice also manifested normal hepatic insulin sensitivity, as assessed by hyperinsulinemic-euglycemic clamps, no PKC epsilon activation, and normal hepatic insulin signaling from the insulin receptor through AKT Ser/Thr kinase. In contrast, aged (10-month-old) L-Mttp(-/-) mice exhibited glucose intolerance and hepatic insulin resistance along with an increase in hepatic plasma membrane sn-1,2-DAG content and PKC epsilon activation. Treatment with a functionally liver-targeted mitochondrial uncoupler protected the aged L-Mttp(-/-) mice against the development of hepatic steatosis, increased plasma membrane sn-1,2-DAG content, PKC epsilon activation, and hepatic insulin resistance. Furthermore, increased hepatic insulin sensitivity in the aged controlled-release mitochondrial protonophore-treated L-Mttp(-/-) mice was not associated with any reductions in hepatic ceramide content. Taken together, these data demonstrate that differences in the intracellular compartmentation of sn-1,2-DAGs in the lipid droplet versus plasma membrane explains the dissociation of NAFLD/lipid-induced hepatic insulin resistance in young L-Mttp(-/-) mice as well as the development of lipid-induced hepatic insulin resistance in aged L-Mttp(-/-) miceThis work was supported by National Institutes of Health Grants R01 DK116774, R01 DK119968, R01 DK114793, R01 DK113984, K23 DK10287, P30 DK045735, DK121490, and HL137202 and the Veterans Health Administration Merit Review Awards I01 BX000901 and BX004113. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the U.S. Department of Veterans Affair

    Understanding earthquake hazards in southern California - the "LARSE" project - working toward a safer future for Los Angeles

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    The Los Angeles region is underlain by a network of active faults, including many that are deep and do not break the Earth’s surface. These hidden faults include the previously unknown one responsible for the devastating January 1994 Northridge earthquake, the costliest quake in U.S. history. So that structures can be built or strengthened to withstand the quakes that are certain in the future, the Los Angeles Region Seismic Experiment (LARSE) is locating hidden earthquake hazards beneath the region to help scientists determine where the strongest shaking will occur
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