Open AccessHeat stress increases insulin sensitivity in pigs
Author(s) -
Sanz Fernandez M. Victoria,
Stoakes Sara K.,
Abuajamieh Mohannad,
Seibert Jacob T.,
Johnson Jay S.,
Horst Erin A.,
Rhoads Robert P.,
Baumgard Lance H.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12478
Subject(s) - medicine , insulin , endocrinology , adipose tissue , basal (medicine) , homeostasis , glucose homeostasis , insulin receptor , insulin resistance , skeletal muscle , glucose uptake , biology , chemistry
Proper insulin homeostasis appears critical for adapting to and surviving a heat load. Further, heat stress ( HS ) induces phenotypic changes in livestock that suggest an increase in insulin action. The current study objective was to evaluate the effects of HS on whole‐body insulin sensitivity. Female pigs (57 ± 4 kg body weight) were subjected to two experimental periods. During period 1, all pigs remained in thermoneutral conditions ( TN ; 21°C) and were fed ad libitum. During period 2, pigs were exposed to: (i) constant HS conditions (32°C) and fed ad libitum ( n = 6), or (ii) TN conditions and pair‐fed ( PFTN ; n = 6) to eliminate the confounding effects of dissimilar feed intake. A hyperinsulinemic euglycemic clamp ( HEC ) was conducted on d3 of both periods; and skeletal muscle and adipose tissue biopsies were collected prior to and after an insulin tolerance test ( ITT ) on d5 of period 2. During the HEC , insulin infusion increased circulating insulin and decreased plasma C‐peptide and nonesterified fatty acids, similarly between treatments. From period 1 to 2, the rate of glucose infusion in response to the HEC remained similar in HS pigs while it decreased (36%) in PFTN controls. Prior to the ITT , HS increased (41%) skeletal muscle insulin receptor substrate‐1 protein abundance, but did not affect protein kinase B or their phosphorylated forms. In adipose tissue, HS did not alter any of the basal or stimulated measured insulin signaling markers. In summary, HS increases whole‐body insulin‐stimulated glucose uptake.