title: Liver but not adipose tissue is responsive to the pattern of enteral feeding.
abstract: Nutritional support is an important aspect of medical care, providing calories to patients with compromised nutrient intake. Metabolism has a diurnal pattern, responding to the light cycle and food intake, which in turn can drive changes in liver and adipose tissue metabolism. In this study, we assessed the response of liver and white adipose tissue (WAT) to different feeding patterns under nutritional support (total enteral nutrition or TEN). Mice received continuous isocaloric TEN for 10 days or equal calories of chow once a day (Ch). TEN was given either at a constant (CN, same infusion rate during 24 h) or variable rate (VN, 80% of calories fed at night, 20% at day). Hepatic lipogenesis and carbohydrate-responsive element-binding protein (ChREBP) expression increased in parallel with the diurnal feeding pattern. Relative to Ch, both patterns of enteral feeding increased adiposity. This increase was not associated with enhanced lipogenic gene expression in WAT; moreover, lipogenesis was unaffected by the feeding pattern. Surprisingly, leptin and adiponectin expression increased. Moreover, nutritional support markedly increased hepatic and adipose FGF21 expression in CN and VN, despite being considered a fasting hormone. In summary, liver but not WAT, respond to the pattern of feeding. While hepatic lipid metabolism adapts to the pattern of nutrient availability, WAT does not. Moreover, sustained delivery of nutrients in an isocaloric diet can cause adiposity without the proinflammatory state observed in hypercaloric feeding. Thus, the liver but not adipose tissue is responsive to the pattern of feeding behavior.
authors.affiliation: Molecular Physiology and Biophysics Department, School of Medicine, Vanderbilt University, Nashville, Tennessee.
authors.forename: Yolanda F
authors.initials: YF
authors.lastname: Otero
authors.affiliation: Molecular Physiology and Biophysics Department, School of Medicine, Vanderbilt University, Nashville, Tennessee.
authors.forename: Tammy M
authors.initials: TM
authors.lastname: Lundblad
authors.affiliation: Molecular Physiology and Biophysics Department, School of Medicine, Vanderbilt University, Nashville, Tennessee ; College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Eric A
authors.initials: EA
authors.lastname: Ford
authors.affiliation: Molecular Physiology and Biophysics Department, School of Medicine, Vanderbilt University, Nashville, Tennessee ; College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Lawrence M
authors.initials: LM
authors.lastname: House
authors.affiliation: Molecular Physiology and Biophysics Department, School of Medicine, Vanderbilt University, Nashville, Tennessee.
authors.forename: Owen P
authors.initials: OP
authors.lastname: McGuinness
keywords: Enteral delivery; feeding pattern; lipogenesis; nutritional support
references.citation: Adv Drug Deliv Rev. 2010 Jul 31;62(9-10):904-17
references.pmid: 20542067
references.citation: Adv Nutr. 2011 Jul;2(4):304-16
references.pmid: 22332072
references.citation: Anal Biochem. 1976 May 7;72:248-54
references.pmid: 942051
references.citation: PLoS One. 2012;7(11):e49993
references.pmid: 23166806
references.citation: Proc Natl Acad Sci U S A. 2009 Dec 29;106(52):22510-5
references.pmid: 20018698
references.citation: Clin Nutr. 2003 Jun;22(3):235-9
references.pmid: 12765661
references.citation: Front Immunol. 2012 Aug 20;3:257
references.pmid: 22934096
references.citation: Curr Opin Pediatr. 2012 Aug;24(4):523-9
references.pmid: 22732636
references.citation: Diabetes. 2010 Apr;59(4):861-71
references.pmid: 20103705
references.citation: PLoS One. 2011;6(8):e22976
references.pmid: 21829679
references.citation: Biochimie. 2012 Oct;94(10):2126-30
references.pmid: 22342903
references.citation: Cell Metab. 2012 Jun 6;15(6):848-60
references.pmid: 22608008
references.citation: Am J Physiol Regul Integr Comp Physiol. 2005 Nov;289(5):R1319-27
references.pmid: 15994371
references.citation: Endocrinology. 2009 Sep;150(9):4084-93
references.pmid: 19470704
references.citation: Cell Metab. 2013 May 7;17(5):790-7
references.pmid: 23663742
references.citation: Am J Physiol Endocrinol Metab. 2005 Jan;288(1):E163-70
references.pmid: 15339746
references.citation: Proc Natl Acad Sci U S A. 2009 Dec 15;106(50):21453-8
references.pmid: 19940241
references.citation: J Biol Chem. 2010 Apr 23;285(17):12851-61
references.pmid: 20178984
references.citation: Endocrinology. 2012 Feb;153(2):690-9
references.pmid: 22147018
references.citation: J Lipid Res. 2012 Aug;53(8):1679-89
references.pmid: 22556214
references.citation: Nutr Hosp. 2011 Nov;26 Suppl 2:46-9
references.pmid: 22411519
references.citation: Pflugers Arch. 2008 Aug;456(5):825-36
references.pmid: 18493788
references.citation: JPEN J Parenter Enteral Nutr. 2000 Sep-Oct;24(5):255-60
references.pmid: 11011779
references.citation: Endocrinology. 2012 May;153(5):2198-207
references.pmid: 22374972
references.citation: Cell Metab. 2013 May 7;17(5):779-89
references.pmid: 23663741
references.citation: Diabetes Res Clin Pract. 2009 Jun;84(3):259-66
references.pmid: 19307037
references.citation: J Lipid Res. 2013 Jan;54(1):152-63
references.pmid: 23103474
references.citation: Cell Metab. 2007 Jun;5(6):426-37
references.pmid: 17550778
references.citation: Endocrinology. 2010 Jan;151(1):153-64
references.pmid: 19880807
references.citation: Proc Natl Acad Sci U S A. 2009 Jun 30;106(26):10853-8
references.pmid: 19541642
references.citation: JPEN J Parenter Enteral Nutr. 2013 Jan;37(1):23-36
references.pmid: 22753619
references.citation: Prostaglandins Leukot Essent Fatty Acids. 2005 Jul;73(1):65-75
references.pmid: 15936183
references.citation: Endocrinology. 2009 Dec;150(12):5341-50
references.pmid: 19837871