Understanding satisfaction of nutrition education and other services provided in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) is needed to ensure the program is responsive to the needs of diverse populations. This study examined the variation of WIC participants’ perceptions and satisfaction with WIC nutrition education and services by race, ethnicity, and language preference. Phone surveys were conducted in 2019 with California WIC families with children aged 1−4 years.
View Article and Find Full Text PDFIn the majority of human cancer cells, cellular immortalization depends on the maintenance of telomere length by telomerase. An essential step required for telomerase function is its recruitment to telomeres, which is regulated by the interaction of the telomere protein, TPP1, with the telomerase essential N-terminal (TEN) domain of the human telomerase reverse transcriptase, hTERT. We previously reported that the hTERT 'insertion in fingers domain' (IFD) recruits telomerase to telomeres in a TPP1-dependent manner.
View Article and Find Full Text PDFThe maintenance of telomeres, which are specialized stretches of DNA found at the ends of linear chromosomes, is a crucial step for the immortalization of cancer cells. Approximately 10-15 % of cancer cells use a homologous recombination-based mechanism known as the Alternative Lengthening of Telomeres (ALT) pathway to maintain their telomeres. Telomeres in general pose a challenge to DNA replication owing to their repetitive nature and potential for forming secondary structures.
View Article and Find Full Text PDFOur group recently documented that male mice containing a deletion for one copy of the gene were completely protected from developing diet-induced obesity (DIO). Here, we conducted a similar investigation but with female littermates. In comparison to our recent publication using male mice, exposure of WT and GRX2+/- female mice to a HFD from 3-to-10 weeks of age did not induce any changes in body mass, circulating blood glucose, food intake, hepatic glycogen levels, or abdominal fat pad mass.
View Article and Find Full Text PDFBackground: Type 2 diabetes (T2D) increases risk for cardiovascular disease. Of interest, liraglutide, a therapy for T2D that activates the glucagon-like peptide-1 receptor to augment insulin secretion, reduces cardiovascular-related death in people with T2D, though it remains unknown how liraglutide produces these actions. Notably, the glucagon-like peptide-1 receptor is not expressed in ventricular cardiac myocytes, making it likely that ventricular myocardium-independent actions are involved.
View Article and Find Full Text PDFHere, we demonstrate that the upregulation of catalase is required to compensate for the loss of nicotinamide nucleotide transhydrogenase (NNT) to maintain hydrogen peroxide (HO) steady-state levels in C57BL/6J liver mitochondria. Our investigations using the closely related mouse strains C57BL/6NJ (6NJ; +NNT) and C57BL/6J (6J; -NNT) revealed that NNT is required for the provision of NADPH and that the upregulation of isocitrate dehydrogenase-2 (IDH2) activity is not enough to compensate for the absence of NNT, which is consistent with previous observations. Intriguingly, despite the absence of NNT, 6J mitochondria had rates of HO production (58.
View Article and Find Full Text PDFResearch over the past seventy years has established that mitochondrial-l-lactate dehydrogenase (m-L-LDH) is vital for mitochondrial bioenergetics. However, in recent report, Fulghum et al. concluded that lactate is a poor fuel for mitochondrial respiration [1].
View Article and Find Full Text PDFOur group recently published a study demonstrating that deleting the gene encoding the matrix thiol oxidoreductase, glutaredoxin-2 (GRX2), alters the bioenergetics of mitochondria isolated from male C57BL/6N mice. Here, we conducted a similar study, examining HO production and respiration in mitochondria isolated from female mice heterozygous (GRX2+/-) or homozygous (GRX2-/-) for glutaredoxin-2. First, we observed that deleting the gene does not alter the rate of HO production in liver and muscle mitochondria oxidizing pyruvate, α-ketoglutarate, or succinate.
View Article and Find Full Text PDFThe aim of this study was to determine whether deleting the gene encoding glutaredoxin-2 (GRX2) could protect mice from diet-induced weight gain. Subjecting wild-type littermates to a high fat diet (HFD) induced a significant increase in overall body mass, white adipose tissue hypertrophy, lipid droplet accumulation in hepatocytes, and higher circulating insulin and triglyceride levels. In contrast, GRX2 heterozygotes (GRX2) fed an HFD had a body mass, white adipose tissue weight, and hepatic and circulating lipid and insulin levels similar to littermates fed a control diet.
View Article and Find Full Text PDFHere, we examined the hydrogen peroxide (HO) producing capacities of pyruvate dehydrogenase (PDH), α-ketoglutarate dehydrogenase (KGDH), proline dehydrogenase (PRODH), glycerol-3-phosphate dehydrogenase (G3PDH), succinate dehydrogenase (SDH; complex II), and branched-chain keto acid dehydrogenase (BCKDH), in cardiac and liver mitochondria isolated from C57BL/6N (6N) and C57BL/6J (6J) mice. Various inhibitor combinations were used to suppress ROS production by complexes I, II, and III and estimate the native rates of HO production for these enzymes. Overall, liver mitochondria from 6N mice produced ∼2-fold more ROS than samples enriched from 6J mice.
View Article and Find Full Text PDFProtein S-glutathionylation reactions are a ubiquitous oxidative modification required to control protein function in response to changes in redox buffering capacity. These reactions are rapid and reversible and are, for the most part, enzymatically mediated by glutaredoxins (GRX) and glutathione S-transferases (GST). Protein S-glutathionylation has been found to control a range of cell functions in response to different physiological cues.
View Article and Find Full Text PDFIt has been reported that mitochondria can contain up to 12 enzymatic sources of reactive oxygen species (ROS). A majority of these sites include flavin-dependent respiratory complexes and dehydrogenases that produce a mixture of superoxide (O2) and hydrogen peroxide (H2O2). Accurate quantification of the ROS-producing potential of individual sites in isolated mitochondria can be challenging due to the presence of antioxidant defense systems and side reactions that also form O2/H2O2.
View Article and Find Full Text PDFProtein S-glutathionylation is a reversible redox modification that regulates mitochondrial metabolism and reactive oxygen species (ROS) production in liver and cardiac tissue. However, whether or not it controls ROS release from skeletal muscle mitochondria has not been explored. In the present study, we examined if chemically-induced protein S-glutathionylation could alter superoxide (O2●-)/hydrogen peroxide (H2O2) release from isolated muscle mitochondria.
View Article and Find Full Text PDFHere, we found that formate, an essential one-carbon metabolite, activates superoxide (O2·-)/hydrogen peroxide (H O ) release from mitochondria. Sodium formate (30 μm) induces a significant increase in O2·-/H O production in liver mitochondria metabolizing pyruvate (50 μm). At concentrations deemed to be toxic, formate does not increase O2·-/H O production further.
View Article and Find Full Text PDFBiochim Biophys Acta Gen Subj
August 2017
Pyruvate dehydrogenase (PDHC) and α-ketoglutarate dehydrogenase complex (KGDHC) are important sources of reactive oxygen species (ROS). In addition, it has been found that mitochondria can also serve as sinks for cellular hydrogen peroxide (HO). However, the ROS forming and quenching capacity of liver mitochondria has never been thoroughly examined.
View Article and Find Full Text PDFHere, we report that choline and dimethylglycine can stimulate reactive oxygen species (ROS) production in liver mitochondria. Choline stimulated O ˙ /H O formation at a concentration of 5 μm. We also observed that Complex II and III inhibitors, atpenin A5 and myxothiazol, collectively induced a 95% decrease in O ˙ /H O production indicating both sites serve as the main sources of ROS during choline oxidation.
View Article and Find Full Text PDFWe tested hypotheses on how animals should respond to heterospecifics encountered in the environment. Hypotheses were formulated from models parameterized to emphasize four factors that are expected to influence species discrimination: mating and territorial interactions; sex differences in resource value; environments in which heterospecifics were common or rare; and the type of identity cues available for species recognition. We also considered the role of phylogeny on contemporary responses to heterospecifics.
View Article and Find Full Text PDFGenetic variation in Avpr1a, the locus encoding the arginine vasopressin receptor 1A (V1aR), has been implicated in pair-bonding behavior in voles (genus Microtus) and humans, raising the possibility that this gene may contribute commonly to mating-system variation in mammals. In voles, differential expression of V1aR in the brain is associated with male partner-preference behavior in a comparison of a monogamous (Microtus ochrogaster) and promiscuous (Microtus montanus) species. This expression difference is correlated, in turn, with a difference in length of a 5' regulatory microsatellite in Avpr1a.
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