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Journal articles on the topic 'Metabolic function'

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1

Morselli, Lisa L., Aurore Guyon, and Karine Spiegel. "Sleep and metabolic function." Pflügers Archiv - European Journal of Physiology 463, no. 1 (November 19, 2011): 139–60. http://dx.doi.org/10.1007/s00424-011-1053-z.

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2

Pandit, Abha, and Abhay Kumar Pandey. "Glycaemic regulation and metabolic syndrome: A reference to thyroid function state." Scholars Journal of Applied Medical Sciences 4, no. 6 (June 2016): 1906–8. http://dx.doi.org/10.21276/sjams.2016.4.6.7.

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3

Brockmöller, Jürgen, and Ivar Roots. "Assessment of Liver Metabolic Function." Clinical Pharmacokinetics 27, no. 3 (September 1994): 216–48. http://dx.doi.org/10.2165/00003088-199427030-00005.

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4

Gutch, Manish, Pankaj Agarwal, and MohitMohan Singh. "Thyroid function and metabolic syndrome." Thyroid Research and Practice 12, no. 3 (2015): 85. http://dx.doi.org/10.4103/0973-0354.157915.

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5

Zhang, Fengxue, Andrew J. Paterson, Ping Huang, Kai Wang, and Jeffrey E. Kudlow. "Metabolic Control of Proteasome Function." Physiology 22, no. 6 (December 2007): 373–79. http://dx.doi.org/10.1152/physiol.00026.2007.

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Proteasomes are major cellular proteases that are important for protein turnover and cell survival. Dysregulation of proteasome is related to many major human diseases. Regulation of the proteasome is beginning to be understood by the recent findings that proteasomes are modified and regulated by metabolic factors O-GlcNAcylation and PKA phosphorylation.
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6

Petit, P., M. M. Loubati�res-Mariani, S. Keppens, and M. J. Sheehan. "Purinergic receptors and metabolic function." Drug Development Research 39, no. 3-4 (November 1996): 413–25. http://dx.doi.org/10.1002/(sici)1098-2299(199611/12)39:3/4<413::aid-ddr23>3.0.co;2-0.

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7

Willis, R. "Metabolic control of heart function." Journal of Molecular and Cellular Cardiology 22, no. 9 (September 1990): x. http://dx.doi.org/10.1016/0022-2828(90)91073-g.

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8

Deeney, Jude T., Marc Prentki, and Barbara E. Corkey. "Metabolic control ofβ-cell function." Seminars in Cell & Developmental Biology 11, no. 4 (August 2000): 267–75. http://dx.doi.org/10.1006/scdb.2000.0175.

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9

Chugh, ShantiN, Kiran Chugh, Sandeep Goyal, and Vijay Shankar. "Thyroid function tests in metabolic syndrome." Indian Journal of Endocrinology and Metabolism 16, no. 6 (2012): 958. http://dx.doi.org/10.4103/2230-8210.102999.

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10

Pouryaghoub, Gholamreza, Ramin Mehrdad, and Mohammad Mehraban. "Metabolic Syndrome and Pulmonary Function Indices." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 25, no. 3 (September 1, 2018): 261–69. http://dx.doi.org/10.2478/rjdnmd-2018-0030.

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Abstract Background and aims: Metabolic syndrome (MetS) is a collection of metabolic risk factors including increased waist circumference (WC), elevated blood pressure (BP), increased triglyceride (TG), decreased high density lipoprotein (HDL-C) and increased fasting blood sugar (FBS). We aimed to examine the relevance between the MetS and its components with reduced lung functions in adult men. Material and method: A total of 3899 adult men underwent screening examination between 2015-2016 in a cross-sectional survey. Results: The mean (± SD) age of our population was 37.25 (± 4.9) years. The overall prevalence of MetS was 7.6%. The total prevalence of reduced lung function in men with MetS was 13.8%. The most common type of reduced lung function was the restrictive pattern (7.1%). The forced expiratory volume of first second (FEV1) and forced vital capacity (FVC) values were significantly lower in men with MetS (both p<0.001). Also these values were significantly lower in diabetic men compared to non-diabetics and those with impaired fasting glucose (IFG). WC and HDL were the most potent predictors of reduced FEV1 and FVC. Conclusions: We obtained a positive independent association between MetS and reduced lung function in adult men which may be related mainly due to increased WC and decreased HDL.
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11

Stranahan, Alexis M., and Mark P. Mattson. "Bidirectional metabolic regulation of neurocognitive function." Neurobiology of Learning and Memory 96, no. 4 (November 2011): 507–16. http://dx.doi.org/10.1016/j.nlm.2011.01.004.

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12

MCNAMARA, DAMIAN. "Euthyroid Function Can Steer Metabolic Syndrome." Family Practice News 37, no. 9 (May 2007): 21. http://dx.doi.org/10.1016/s0300-7073(07)70540-6.

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13

Bugger, Heiko, and E. Dale Abel. "The Metabolic Syndrome and Cardiac Function." Advances in Pulmonary Hypertension 7, no. 3 (August 1, 2008): 332–36. http://dx.doi.org/10.21693/1933-088x-7.3.332.

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14

Scarlata, Simone, Filippo Luca Fimognari, Leo Moro, Ruggiero Pastorelli, and Raffaele Antonelli-Incalzi. "Metabolic Syndrome and Impaired Lung Function." Chest 137, no. 2 (February 2010): 494. http://dx.doi.org/10.1378/chest.09-1539.

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15

Dubé, Nadia, and Michel L. Tremblay. "Beyond the Metabolic Function of PTP1B." Cell Cycle 3, no. 5 (May 2004): 548–51. http://dx.doi.org/10.4161/cc.3.5.851.

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16

Borges, Ricardo, Paulo Temido, Luís Sousa, Paulo Azinhais, Paulo Conceição, Bruno Pereira, Ricardo Leão, et al. "Metabolic Syndrome and Sexual (Dys)function." Journal of Sexual Medicine 6, no. 11 (November 2009): 2958–75. http://dx.doi.org/10.1111/j.1743-6109.2009.01412.x.

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17

Leone, Nathalie, Dominique Courbon, Frédérique Thomas, Kathy Bean, Bertrand Jégo, Bénédicte Leynaert, Louis Guize, and Mahmoud Zureik. "Lung Function Impairment and Metabolic Syndrome." American Journal of Respiratory and Critical Care Medicine 179, no. 6 (March 15, 2009): 509–16. http://dx.doi.org/10.1164/rccm.200807-1195oc.

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18

Burgess, R. J., M. Agathocleous, and S. J. Morrison. "Metabolic regulation of stem cell function." Journal of Internal Medicine 276, no. 1 (June 18, 2014): 12–24. http://dx.doi.org/10.1111/joim.12247.

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19

Bui, Bang V., Rebecca G. Hu, Monica L. Acosta, Paul Donaldson, Algis J. Vingrys, and Michael Kalloniatis. "Glutamate metabolic pathways and retinal function." Journal of Neurochemistry 111, no. 2 (October 2009): 589–99. http://dx.doi.org/10.1111/j.1471-4159.2009.06354.x.

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20

Zach, J., and S. H. Ackerman. "Thyroid function, metabolic regulation, and depression." Psychosomatic Medicine 50, no. 5 (September 1988): 454–68. http://dx.doi.org/10.1097/00006842-198809000-00002.

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21

Onuora, Sarah. "Metabolic changes modify Treg cell function." Nature Reviews Rheumatology 12, no. 11 (October 21, 2016): 621. http://dx.doi.org/10.1038/nrrheum.2016.172.

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22

Fitchett, David, and Kim A. Connelly. "Impaired Cardiac Function in Metabolic Syndrome." Canadian Journal of Cardiology 30, no. 3 (March 2014): 270–71. http://dx.doi.org/10.1016/j.cjca.2014.01.012.

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23

Wijnands, W. J. A. "The metabolic function of the lung." Pharmaceutisch Weekblad Scientific Edition 9, no. 2 (April 1987): 61–64. http://dx.doi.org/10.1007/bf01960737.

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24

Holthaus, Lisa, Virag Sharma, Daniel Brandt, Anette-Gabriele Ziegler, Martin Jastroch, and Ezio Bonifacio. "Functional and metabolic fitness of human CD4+ T lymphocytes during metabolic stress." Life Science Alliance 4, no. 12 (September 27, 2021): e202101013. http://dx.doi.org/10.26508/lsa.202101013.

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Human CD4+ T cells are essential mediators of immune responses. By altering the mitochondrial and metabolic states, we defined metabolic requirements of human CD4+ T cells for in vitro activation, expansion, and effector function. T-cell activation and proliferation were reduced by inhibiting oxidative phosphorylation, whereas early cytokine production was maintained by either OXPHOS or glycolytic activity. Glucose deprivation in the presence of mild mitochondrial stress markedly reduced all three T-cell functions, contrasting the exposure to resveratrol, an antioxidant and sirtuin-1 activator, which specifically inhibited cytokine production and T-cell proliferation, but not T-cell activation. Conditions that inhibited T-cell activation were associated with the down-regulation of 2′,5′-oligoadenylate synthetase genes via interferon response pathways. Our findings indicate that T-cell function is grossly impaired by stressors combined with nutrient deprivation, suggesting that correcting nutrient availability, metabolic stress, and/or the function of T cells in these conditions will improve the efficacy of T-cell–based therapies.
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25

Taneja, Charit, Sakshi Gera, Se-Min Kim, Jameel Iqbal, Tony Yuen, and Mone Zaidi. "FSH-metabolic circuitry and menopause." Journal of Molecular Endocrinology 63, no. 3 (October 2019): R73—R80. http://dx.doi.org/10.1530/jme-19-0152.

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FSH has a primary function in procreation, wherein it induces estrogen production in females and regulates spermatogenesis in males. However, in line with our discoveries over the past decade of non-unitary functions of pituitary hormones, we and others have described hitherto uncharacterized functions of FSH. Through high-affinity receptors, some of which are variants of the ovarian FSH receptor (FSHR), FSH regulates bone mass, adipose tissue function, energy metabolism, and cholesterol production in both sexes. These newly described actions of FSH may indeed be relevant to the pathogenesis of bone loss, dysregulated energy homeostasis, and disordered lipid metabolism that accompany the menopause in females and aging in both genders. We are therefore excited about the possibility of modulating circulating FSH levels toward a therapeutic benefit for a host of age-associated diseases, including osteoporosis, obesity and dyslipidemia, among other future possibilities.
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26

Mahadevan, R., and B. O. Palsson. "Properties of Metabolic Networks: Structure versus Function." Biophysical Journal 88, no. 1 (January 2005): L07—L09. http://dx.doi.org/10.1529/biophysj.104.055723.

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27

Kim, Do-Jin, and Jong-Hyuck Kim. "Relationship between Cardiopulmonary function Metabolic Syndrome Indices." Research Journal of Pharmacy and Technology 10, no. 11 (2017): 3868. http://dx.doi.org/10.5958/0974-360x.2017.00702.8.

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28

Kokot, Franciszek, Andrzej Wiecek, and Wladyslaw Grzeszczak. "Endocrine and Metabolic Function in Renal Failure." Seminars in Dialysis 1, no. 4 (October 1, 2007): 213–19. http://dx.doi.org/10.1111/j.1525-139x.1988.tb00731.x.

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29

Ghosh, Siddhartha S., Jing Wang, Paul J. Yannie, and Shobha Ghosh. "Intestinal barrier function and metabolic/liver diseases." Liver Research 4, no. 2 (June 2020): 81–87. http://dx.doi.org/10.1016/j.livres.2020.03.002.

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30

Tai, Hsin-Hsiung, Huiping Zhou, C. Mark Ensor, Fengxiang Yan, Wenjun Kang, and Hepan Tan. "Structure and function of prostaglandin metabolic enzymes." Prostaglandins & Other Lipid Mediators 59, no. 1-6 (December 1999): 99. http://dx.doi.org/10.1016/s0090-6980(99)90334-9.

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31

Ghosh-Choudhary, Shohini, Jie Liu, and Toren Finkel. "Metabolic Regulation of Cell Fate and Function." Trends in Cell Biology 30, no. 3 (March 2020): 201–12. http://dx.doi.org/10.1016/j.tcb.2019.12.005.

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32

Goulis, Dimitrios G., and Basil C. Tarlatzis. "Metabolic syndrome and reproduction: I. Testicular function." Gynecological Endocrinology 24, no. 1 (January 2008): 33–39. http://dx.doi.org/10.1080/09513590701582273.

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33

Watz, Henrik, Benjamin Waschki, Anne Kirsten, Kai-Christian Müller, Gunther Kretschmar, Thorsten Meyer, Olaf Holz, and Helgo Magnussen. "Metabolic Syndrome and Impaired Lung Function: Response." Chest 137, no. 2 (February 2010): 494–95. http://dx.doi.org/10.1378/chest.09-2684.

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34

Aizawa, Kunihiko, J. Kevin Shoemaker, Tom J. Overend, and Robert J. Petrella. "Metabolic syndrome, endothelial function and lifestyle modification." Diabetes and Vascular Disease Research 6, no. 3 (July 2009): 181–89. http://dx.doi.org/10.1177/1479164109336375.

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35

Hatzimanikatis, Vassily, Chunhui Li, Justin A. Ionita, and Linda J. Broadbelt. "Metabolic networks: enzyme function and metabolite structure." Current Opinion in Structural Biology 14, no. 3 (June 2004): 300–306. http://dx.doi.org/10.1016/j.sbi.2004.04.004.

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36

Saha, Shilpi, Irina N. Shalova, and Subhra K. Biswas. "Metabolic regulation of macrophage phenotype and function." Immunological Reviews 280, no. 1 (October 13, 2017): 102–11. http://dx.doi.org/10.1111/imr.12603.

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37

Naveed, Bushra, Michael D. Weiden, Sophia Kwon, Edward J. Gracely, Ashley L. Comfort, Natalia Ferrier, Kusali J. Kasturiarachchi, et al. "Metabolic Syndrome Biomarkers Predict Lung Function Impairment." American Journal of Respiratory and Critical Care Medicine 185, no. 4 (February 15, 2012): 392–99. http://dx.doi.org/10.1164/rccm.201109-1672oc.

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38

Levin, Robert M., Niels Haugaard, Joseph A. Hypolite, Alan J. Wein, and Ralph Buttyan. "Metabolic factors influencing lower urinary tract function." Experimental Physiology 84, no. 1 (January 1999): 171–94. http://dx.doi.org/10.1111/j.1469-445x.1999.tb00082.x.

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39

Lee, Richard K., Bilal Chughtai, Alexis E. Te, and Steven A. Kaplan. "Sexual Function in Men with Metabolic Syndrome." Urologic Clinics of North America 39, no. 1 (February 2012): 53–62. http://dx.doi.org/10.1016/j.ucl.2011.09.008.

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40

Arif, Abul, and Paul L. Fox. "Unexpected metabolic function of a tRNA synthetase." Cell Cycle 16, no. 23 (December 2, 2017): 2239–40. http://dx.doi.org/10.1080/15384101.2017.1324127.

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41

Indo, Yoriko, Sunao Takeshita, Kiyo-Aki Ishii, Takayuki Hoshii, Hiroyuki Aburatani, Atsushi Hirao, and Kyoji Ikeda. "Metabolic regulation of osteoclast differentiation and function." Journal of Bone and Mineral Research 28, no. 11 (October 18, 2013): 2392–99. http://dx.doi.org/10.1002/jbmr.1976.

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42

Davis, Timothy ME. "Lung function, diabetes and the metabolic syndrome." Practical Diabetes 31, no. 5 (June 2014): 184–85. http://dx.doi.org/10.1002/pdi.1861.

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43

Chen, Wei-Liang, Chung-Ching Wang, Li-Wei Wu, Tung-Wei Kao, James Yi-Hsin Chan, Ying-Jen Chen, Ya-Hui Yang, Yaw-Wen Chang, and Tao-Chun Peng. "Relationship between Lung Function and Metabolic Syndrome." PLoS ONE 9, no. 10 (October 9, 2014): e108989. http://dx.doi.org/10.1371/journal.pone.0108989.

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44

Cherry-peppers, G., J. Sorkin, R. Andres, B. J. Baum, and J. A. Ship. "Salivary Gland Function and Glucose Metabolic Status." Journal of Gerontology 47, no. 4 (July 1, 1992): M130—M134. http://dx.doi.org/10.1093/geronj/47.4.m130.

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45

Casagrande, Stefania, and Michaela Hau. "Telomere attrition: metabolic regulation and signalling function?" Biology Letters 15, no. 3 (March 2019): 20180885. http://dx.doi.org/10.1098/rsbl.2018.0885.

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Stress exposure can leave long-term footprints within the organism, like in telomeres (TLs), protective chromosome caps that shorten during cell replication and following exposure to stressors. Short TLs are considered to indicate lower fitness prospects, but why TLs shorten under stressful conditions is not understood. Glucocorticoid hormones (GCs) increase upon stress exposure and are thought to promote TL shortening by increasing oxidative damage. However, evidence that GCs are pro-oxidants and oxidative stress is causally linked to TL attrition is mixed . Based on new biochemical findings, we propose the metabolic telomere attrition hypothesis: during times of substantially increased energy demands, TLs are shortened as part of the transition into an organismal ‘emergency state’, which prioritizes immediate survival functions over processes with longer-term benefits. TL attrition during energy shortages could serve multiple roles including amplified signalling of cellular energy debt to re-direct critical resources to immediately important processes. This new view of TL shortening as a strategy to resolve major energetic trade-offs can improve our understanding of TL dynamics. We suggest that TLs are master regulators of cell homeostasis and propose future research avenues to understand the interactions between energy homeostasis, metabolic regulators and TL.
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46

Punjabi, Naresh M. "Improvement of Metabolic Function in Sleep Apnea." American Journal of Respiratory and Critical Care Medicine 169, no. 2 (January 15, 2004): 139–40. http://dx.doi.org/10.1164/rccm.2310017.

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47

Marni, A., M. E. Ferrero, and G. Gaja. "METABOLIC FUNCTION OF GRAFTED LIVER IN RATS." Transplantation 46, no. 6 (December 1988): 830–34. http://dx.doi.org/10.1097/00007890-198812000-00008.

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48

Seidler, Emily, and Kelle Moley. "Metabolic Determinants of Mitochondrial Function in Oocytes." Seminars in Reproductive Medicine 33, no. 06 (November 12, 2015): 396–400. http://dx.doi.org/10.1055/s-0035-1567822.

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49

Afzal, Nasrin, Carmen A. Mannella, W. Jonathan Lederer, and M. Saleet Jafri. "Cardiac Calcium Signaling and Mitochondrial Metabolic Function." Biophysical Journal 116, no. 3 (February 2019): 270a. http://dx.doi.org/10.1016/j.bpj.2018.11.1463.

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50

Duckworth, Benjamin P., and Courtney C. Aldrich. "Assigning Enzyme Function from the Metabolic Milieu." Chemistry & Biology 17, no. 4 (April 2010): 313–14. http://dx.doi.org/10.1016/j.chembiol.2010.04.001.

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