title: A Single Bout of Fasting (24 h) Reduces Basal Cytokine Expression and Minimally Impacts the Sterile Inflammatory Response in the White Adipose Tissue of Normal Weight F344 Rats.
abstract: Sterile inflammation occurs when inflammatory proteins are increased in blood and tissues by nonpathogenic states and is a double-edged sword depending on its cause (stress, injury, or disease), duration (transient versus chronic), and inflammatory milieu. Short-term fasting can exert a host of health benefits through unknown mechanisms. The following experiment tested if a 24 h fast would modulate basal and stress-evoked sterile inflammation in plasma and adipose. Adult male F344 rats were either randomized toad libitumaccess to food or fasted for 24 h prior to 0 (control), 10, or 100, 1.5 mA-5 s intermittent, inescapable tail shocks (IS). Glucose, nonesterified free fatty acids (NEFAs), insulin, leptin, and corticosterone were measured in plasma and tumor necrosis factor- (TNF-)α, interleukin- (IL-) 1β, IL-6, and IL-10 in plasma, and subcutaneous, intraperitoneal, and visceral compartments of white adipose tissue (WAT). In control rats, a 24 h fast reduced all measured basal cytokines in plasma and visceral WAT, IL-1βand IL-6 in subcutaneous WAT, and IL-6 in intraperitoneal WAT. In stressed rats (IS), fasting reduced visceral WAT TNF-α, subcutaneous WAT IL-1β, and plasma insulin and leptin. Short-term fasting may thus prove to be a useful dietary strategy for reducing peripheral inflammatory states associated with visceral obesity and chronic stress.
authors.affiliation: Department of Integrative Physiology, University of Colorado, Boulder, CO, USA.
authors.forename: Kristin J
authors.identifier: 0000-0001-5945-5243
authors.initials: KJ
authors.lastname: Speaker
authors.affiliation: Department of Integrative Physiology, University of Colorado, Boulder, CO, USA.
authors.forename: Madeline M
authors.initials: MM
authors.lastname: Paton
authors.affiliation: Department of Integrative Physiology, University of Colorado, Boulder, CO, USA.
authors.forename: Stewart S
authors.initials: SS
authors.lastname: Cox
authors.affiliation: Department of Integrative Physiology, University of Colorado, Boulder, CO, USA; Center for Neuroscience, University of Colorado, Boulder, CO, USA.
authors.forename: Monika
authors.identifier: 0000-0002-0470-0827
authors.initials: M
authors.lastname: Fleshner
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D003345:Corticosterone / Q000097:blood; D016207:Cytokines / Q000097:blood*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005508:Food Deprivation; D007249:Inflammation / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D011897:Random Allocation; D051381:Rats; D011916:Rats, Inbred F344; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D005230:Fatty Acids, Nonesterified; C000594089:IL1B protein, rat; D007328:Insulin; D053583:Interleukin-1beta; D015850:Interleukin-6; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D003345:Corticosterone