title: Chronic heat stress up-regulates leptin and adiponectin secretion and expression and improves leptin, adiponectin and insulin sensitivity in mice.
abstract: Heat stress (HS) induces adaptive responses that are responsible for alterations of carbohydrate and lipid metabolism. This study aimed to evaluate the effects of chronic heat treatment on the expression and secretion of leptin and adiponectin, important regulators of energy homeostasis, food intake and insulin action. C57BL/6 mice were subdivided into three groups (24 mice each). The first group was kept under control conditions (C: 22±2 °C). The second group was exposed to HS (35±1 °C). The third group was kept under control conditions and was food restricted (FR). The HS group had higher rectal temperature than the C and FR groups and lower food intake than the C group. Hspa1 (Hspa1a) gene expression in adipose tissue, muscle and liver was higher under HS than FR and C. Heat treatment resulted in decreased blood glucose and non-esterified fatty acids; increased leptin, adiponectin and insulin secretion; and greater glucose disposal. Leptin, adiponectin, leptin and adiponectin receptors, insulin receptor substrate-1 and glucose transporter mRNAs were up-regulated in HS mice. This study provides evidence that HS improves leptin and adiponectin signalling in adipose tissue, muscle and liver. Heat stress was responsible for improving insulin sensitivity and glucose uptake in peripheral tissues, probably mediated by adipokines. Changes in the adipokine levels and sensitivity to them may be considered as an adaptive response to heat.
authors.affiliation: Department of Agriculture, Forestry, Nature and Energy, University of Tuscia, via San Camillo De Lellis, SNC 01100 Viterbo, Italy.
authors.forename: Patrizia
authors.initials: P
authors.lastname: Morera
authors.forename: Loredana
authors.initials: L
authors.lastname: Basiricò
authors.forename: Kenji
authors.initials: K
authors.lastname: Hosoda
authors.forename: Umberto
authors.initials: U
authors.lastname: Bernabucci
mesh_terms: D052242:Adiponectin / Q000097:blood / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001831:Body Temperature; D004326:Drinking; D004435:Eating; D005951:Glucose Tolerance Test; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D018869:Heat-Shock Response / Q000502:physiology*; D006358:Hot Temperature; D006801:Humans; D007328:Insulin / Q000378:metabolism; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D000078790:Insulin Secretion; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000648:ultrastructure; D020738:Leptin / Q000097:blood / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D054419:Receptors, Adiponectin / Q000235:genetics / Q000378:metabolism; D054411:Receptors, Leptin / Q000235:genetics / Q000378:metabolism; D013312:Stress, Physiological; D015854:Up-Regulation
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D051246:Glucose Transport Proteins, Facilitative; D018840:HSP70 Heat-Shock Proteins; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; C526295:Irs1 protein, mouse; D020738:Leptin; D054419:Receptors, Adiponectin; D054411:Receptors, Leptin