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  • American Physiological Society  (12)
  • 1
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    Online Resource
    Template to improve glycemic control without reducing adiposity or dietary fat
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 300, No. 5 ( 2011-05), p. E779-E789
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 300, No. 5 ( 2011-05), p. E779-E789
    Abstract: Drugs that improve chronic hyperglycemia independently of insulin signaling or reduction of adiposity or dietary fat intake may be highly desirable. Ad36, a human adenovirus, promotes glucose uptake in vitro independently of adiposity or proximal insulin signaling. We tested the ability of Ad36 to improve glycemic control in vivo and determined if the natural Ad36 infection in humans is associated with better glycemic control. C57BL/6J mice fed a chow diet or made diabetic with a high-fat (HF) diet were mock infected or infected with Ad36 or adenovirus Ad2 as a control for infection. Postinfection (pi), systemic glycemic control, hepatic lipid content, and cell signaling in tissues pertinent to glucose metabolism were determined. Next, sera of 1,507 adults and children were screened for Ad36 antibodies as an indicator of past natural infection. In chow-fed mice, Ad36 significantly improved glycemic control for 12 wk pi. In HF-fed mice, Ad36 improved glycemic control and hepatic steatosis up to 20 wk pi. In adipose tissue (AT), skeletal muscle (SM), and liver, Ad36 upregulated distal insulin signaling without recruiting the proximal insulin signaling. Cell signaling suggested that Ad36 increases AT and SM glucose uptake and reduces hepatic glucose release. In humans, Ad36 infection predicted better glycemic control and lower hepatic lipid content independently of age, sex, or adiposity. We conclude that Ad36 offers a novel tool to understand the pathways to improve hyperglycemia and hepatic steatosis independently of proximal insulin signaling, and despite a HF diet. This metabolic engineering by Ad36 appears relevant to humans for developing more practical and effective antidiabetic approaches.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00703.2010
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 2
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    Alterations in carbohydrate metabolism and its regulation in PPARα null mouse hearts
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 294, No. 4 ( 2008-04), p. H1571-H1580
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 294, No. 4 ( 2008-04), p. H1571-H1580
    Abstract: Although a shift from fatty acids (FAs) to carbohydrates (CHOs) is considered beneficial for the diseased heart, it is unclear why subjects with FA β-oxidation defects are prone to cardiac decompensation under stress conditions. The present study investigated potential alterations in the myocardial utilization of CHOs for energy production and anaplerosis in 12-wk-old peroxisome proliferator-activating receptor-α (PPARα) null mice (a model of FA β-oxidation defects). Carbon-13 methodology was used to assess substrate flux through energy-yielding pathways in hearts perfused ex vivo at two workloads with a physiological substrate mixture mimicking the fed state, and real-time RT-quantitative polymerase chain reaction was used to document the expression of selected metabolic genes. When compared with that from control C57BL/6 mice, isolated working hearts from PPARα null mice displayed an impaired capacity to withstand a rise in preload (mimicking an increased venous return as it occurs during exercise) as reflected by a 20% decline in the aortic flow rate. At the metabolic level, beyond the expected shift from FA (5-fold down) to CHO (1.5-fold up; P 〈 0.001) at both preloads, PPARα null hearts also displayed 1) a significantly greater contribution of exogenous lactate and glucose and/or glycogen (2-fold up) to endogenous pyruvate formation, whereas that of exogenous pyruvate remained unchanged and 2) marginal alterations in citric acid cycle-related parameters. The lactate production rate was the only measured parameter that was affected differently by preloads in control and PPARα null mouse hearts, suggesting a restricted reserve for the latter hearts to enhance glycolysis when the energy demand is increased. Alterations in the expression of some glycolysis-related genes suggest potential mechanisms involved in this defective CHO metabolism. Collectively, our data highlight the importance of metabolic alterations in CHO metabolism associated with FA oxidation defects as a factor that may predispose the heart to decompensation under stress conditions even in the fed state.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01340.2007
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477308-9
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  • 3
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    Online Resource
    Probing the link between citrate and malonyl-CoA in perfused rat hearts
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 283, No. 4 ( 2002-10-01), p. H1379-H1386
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 283, No. 4 ( 2002-10-01), p. H1379-H1386
    Abstract: Little is known about the sources of cytosolic acetyl-CoA used for the synthesis of malonyl-CoA, a key regulator of fatty acid oxidation in the heart. We tested the hypothesis that citrate provides acetyl-CoA for malonyl-CoA synthesis after its mitochondrial efflux and cleavage by cytosolic ATP-citrate lyase. We expanded on a previous study where we characterized citrate release from perfused rat hearts (Vincent G, Comte B, Poirier M, and Des Rosiers C. Citrate release by perfused rat hearts: a window on mitochondrial cataplerosis. Am J Physiol Endocrinol Metab 278: E846–E856, 2000). In the present study, we show that citrate release rates, ranging from 6 to 22 nmol/min, can support a net increase in malonyl-CoA concentrations induced by changes in substrate supply, at most 0.7 nmol/min. In experiments with [U- 13 C](lactate + pyruvate) and [1- 13 C]oleate, we show that the acetyl moiety of malonyl-CoA is derived from both pyruvate and long-chain fatty acids. This 13 C-labeling of malonyl-CoA occurred without any changes in its concentration. Hydroxycitrate, an inhibitor of ATP-citrate lyase, prevents increases in malonyl-CoA concentrations and decreases its labeling from [U- 13 C](lactate + pyruvate). Our data support at least a partial role of citrate in the transfer from the mitochondria to cytosol of acetyl units for malonyl-CoA synthesis. In addition, they provide a dynamic picture of malonyl-CoA metabolism: even when the malonyl-CoA concentration remains constant, there appears to be a constant need to supply acetyl-CoA from various carbon sources, both carbohydrates and lipids, for malonyl-CoA synthesis.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00244.2002
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477308-9
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  • 4
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    Online Resource
    Major gene effects on exercise ventilatory threshold: the HERITAGE Family Study
    American Physiological Society ; 2002
    In:  Journal of Applied Physiology Vol. 93, No. 3 ( 2002-09-01), p. 1000-1006
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 93, No. 3 ( 2002-09-01), p. 1000-1006
    Abstract: This study investigates whether there are major gene effects on oxygen uptake at the ventilatory threshold (V˙o 2 VT ) and theV˙o 2 VT maximal oxygen uptake (VT%V˙o 2 max ), at baseline and in response to 20 wk of exercise training by using data on 336 whites and 160 blacks. Segregation analysis was performed on the residuals ofV˙o 2 VT and VT%V˙o 2 max . In whites, there was strong evidence of a major gene, with 3 and 2% of the sample in the upper distribution, that accounted for 52 and 43% of the variance in baseline V˙o 2 VT and VT%V˙o 2 max , respectively. There were no genotype-specific covariate effects (sex, age, weight, fat mass, and fat-free mass). The segregation results were inconclusive for the training response in whites, and for the baseline and training response in blacks, probably due to insufficient power because of reduced sample sizes or smaller gene effect or both. The strength of the genetic evidence for V˙o 2 VT and VT%V˙o 2 max suggests that these traits should be further investigated for potential relations with specific candidate genes, if they can be identified, and explored through a genome-wide scan.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00254.2002
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
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    Heredity and overfeeding-induced changes in submaximal exercise VO2
    American Physiological Society ; 1987
    In:  Journal of Applied Physiology Vol. 62, No. 2 ( 1987-02-01), p. 539-544
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 62, No. 2 ( 1987-02-01), p. 539-544
    Abstract: The present study investigated the role of heredity in determining changes in the energy cost of submaximal exercise in response to short-term overfeeding. Six pairs of monozygotic twins were subjected to a 1,000 kcal/day surplus for 22 days with careful experimental controls over food intake and physical activities. O2 consumption (VO2) was measured during a submaximal treadmill exercise test 165 min postprandially before and the morning after the overfeeding protocol. As expected, overfeeding induced significant increases in body weight and fat mass. No significant increase in mean exercise VO2 was observed after overfeeding. However, the interindividual variation in overfeeding-induced changes in exercise VO2 was large and not randomly distributed. When comparing intrapair variance for changes in exercise VO2 to interpair variance, a moderate to high within-pair resemblance in response, i.e., a genotype-overfeeding interaction, was observed. Changes in exercise VO2 were positively correlated with those in postexercise levels of blood catecholamines, particularly epinephrine. A negative correlation was found between changes in exercise VO2 and body fat gain. These results are consistent with the concept of a role for the sympathoadrenal system in the regulation of adaptive thermogenesis and the predisposition to store fat. Moreover, these data suggest that the sensitivity to adapt in exercise energy expenditure after overfeeding is inherited to a significant extent.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1987.62.2.539
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 6
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    Genotype dependency of adaptation in adipose tissue metabolism after short-term overfeeding
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 250, No. 4 ( 1986-04-01), p. E480-E485
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 250, No. 4 ( 1986-04-01), p. E480-E485
    Abstract: The present study investigated the interaction of genotype and short-term overfeeding on adipose tissue metabolism of six pairs of male monozygotic twins. The sedentary nonobese twins were submitted to a 22-day overfeeding period in which their normal daily intake was supplemented by an additional 1,000 kcal/day. A fat tissue biopsy was performed in the suprailiac region before and after overfeeding to determine fat cell diameter and basal and maximal stimulated epinephrine, norepinephrine, and isoproterenol lipolysis from collagenase-isolated fat cells. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides (basal and stimulated lipogenesis) were measured using [14C]glucose. Adipose tissue heparin-releasable lipoprotein lipase activity (LPL) was also determined. A repeated measures analysis of variance revealed overfeeding induced significant elevations in basal lipogenesis (P less than 0.05) and fat cell diameter (P less than 0.05). No significant group changes were noted in basal, epinephrine-, norepinephrine-, and isoproterenol-stimulated lipolysis, insulin-stimulated lipogenesis, and LPL activity due to large individual variation in the response to overfeeding. However, significant intrapair resemblance was noted in the changes of the aforementioned variables, suggesting a coherent within-twin pair response, despite large between-pair variation in response. Less within-pair similarity was noted in changes in basal lipogenesis and fat cell diameter. The results of the present study suggest that overfeeding induced a large range of adipose tissue metabolic responses and that the genotype plays a role in determining the sensitivity of adipose tissue adaptation to caloric affluence.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1986.250.4.E480
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477331-4
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  • 7
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    Functional desensitization to isoproterenol without reducing cAMP production in canine failing cardiocytes
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 280, No. 2 ( 2001-02-01), p. R355-R364
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 280, No. 2 ( 2001-02-01), p. R355-R364
    Abstract: To corroborate alterations in the functional responses to β-adrenergic receptor (β-AR) stimulation with changes in β-AR signaling in failing cardiomyocytes, contractile and L-type Ca 2+ current responses to isoproterenol along with stimulated cAMP generation were compared among cardiomyocytes isolated from canines with tachycardia-induced heart failure or healthy hearts. The magnitude of shortening of failing cardiomyocytes was significantly depressed (by 22 ± 4.4%) under basal conditions, and the maximal response to isoproterenol was significantly reduced (by 45 ± 18%). Similar results were obtained when the responses in the rate of contraction and rate of relaxation to isoproterenol were considered. The L-type Ca 2+ current amplitude measured in failing cardiomyocytes under basal conditions was unchanged, but the responses to isoproterenol were significantly reduced compared with healthy cells. Isoproterenol-stimulated cAMP generation was similar in sarcolemmal membranes derived from the homogenates of failing (45 ± 6.8) and healthy cardiomyocytes (52 ± 8.5 pmol cAMP · mg protein −1 · min −1 ). However, stimulated cAMP generation was found to be significantly reduced when the membranes were derived from the homogenates of whole tissue (failing: 67 ± 8.1 vs. healthy: 140 ± 27.8 pmol cAMP · mg protein −1 · min −1 ). Total β-AR density was not reduced in membranes derived from either whole tissue or isolated cardiomyocyte homogenates, but the β 1 /β 2 ratio was significantly reduced in the former (failing: 45/55 vs. healthy: 72/28) without being altered in the latter (failing: 72/28, healthy: 77/23). We thus conclude that, in tachycardia-induced heart failure, reduction in the functional responses of isolated cardiomyocytes to β-AR stimulation may be attributed to alterations in the excitation-contraction machinery rather than to limitation of cAMP generation.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2001.280.2.R355
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 8
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    Myocardial oxygenation is critical for improving regeneration capacity
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 296, No. 5 ( 2009-05), p. H1215-H1216
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 296, No. 5 ( 2009-05), p. H1215-H1216
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00258.2009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
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    Omics-driven investigation of the biology underlying intrinsic submaximal working capacity and its trainability
    American Physiological Society ; 2023
    In:  Physiological Genomics Vol. 55, No. 11 ( 2023-11-01), p. 517-543
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 55, No. 11 ( 2023-11-01), p. 517-543
    Abstract: Submaximal exercise capacity is an indicator of cardiorespiratory fitness with clinical and public health implications. Submaximal exercise capacity and its response to exercise programs are characterized by heritability levels of about 40%. Using physical working capacity (power output) at a heart rate of 150 beats/min (PWC150) as an indicator of submaximal exercise capacity in subjects of the HERITAGE Family Study, we have undertaken multi-omics and in silico explorations of the underlying biology of PWC150 and its response to 20 wk of endurance training. Our goal was to illuminate the biological processes and identify panels of genes associated with human variability in intrinsic PWC150 (iPWC150) and its trainability (dPWC150). Our bioinformatics approach was based on a combination of genome-wide association, skeletal muscle gene expression, and plasma proteomics and metabolomics experiments. Genes, proteins, and metabolites showing significant associations with iPWC150 or dPWC150 were further queried for the enrichment of biological pathways. We compared genotype-phenotype associations of emerging candidate genes with reported functional consequences of gene knockouts in mouse models. We investigated the associations between DNA variants and multiple muscle and cardiovascular phenotypes measured in HERITAGE subjects. Two panels of prioritized genes of biological relevance to iPWC150 (13 genes) and dPWC150 (6 genes) were identified, supporting the hypothesis that genes and pathways associated with iPWC150 are different from those underlying dPWC150. Finally, the functions of these genes and pathways suggested that human variation in submaximal exercise capacity is mainly driven by skeletal muscle morphology and metabolism and red blood cell oxygen-carrying capacity. NEW & NOTEWORTHY Multi-omics and in silico explorations of the genes and underlying biology of submaximal exercise capacity and its response to 20 wk of endurance training were undertaken. Prioritized genes were identified: 13 genes for variation in submaximal exercise capacity in the sedentary state and 5 genes for the response level to endurance training, with no overlap between them. Genes and pathways associated with submaximal exercise capacity in the sedentary state are different from those underlying trainability.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00163.2022
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 2031330-5
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  • 10
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    Heredity and changes in hormones and metabolic rates with short-term training
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 250, No. 6 ( 1986-06-01), p. E711-E717
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 250, No. 6 ( 1986-06-01), p. E711-E717
    Abstract: The purpose of this experiment was to assess the effects of a 22-day training program on resting metabolic rate (RMR), thermic effect of a meal (TEM), and associated hormonal changes. Six pairs of male monozygotic twins were submitted to a 22-day ergocycle exercise program designed to induce a deficit in energy balance of 4.2 MJ per day. RMR and TEM after a 4.2-MJ meal challenge were measured before and after training. Results indicated that RMR and TEM did not change significantly, although a large variation in response between twin pairs was observed. Moreover, training reduced (P less than 0.05) basal and postprandial insulin response, plasma thyroid hormones triiodothyronine (T3), thyroxine (T4), and FT4 (P less than 0.05). Absolute changes in RMR and TEM exhibited significant within-pair resemblance in response, with intraclass correlations reaching r = 0.81 (P less than 0.05) and r = 0.72 (P less than 0.05), respectively. Changes in T4 and FT4 also exhibited moderate within-pair resemblance (0.42 less than or equal to r less than or equal to 0.71). These results suggest that short-term exercise training does not modify RMR and TEM but can significantly decrease plasma levels of insulin and thyroid hormones. Moreover, the similarity of response within twin pairs suggests that heredity plays a role in determining RMR, TEM, and thyroid hormone adaptation to exercise training generating a negative energy balance.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1986.250.6.E711
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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