An acute bout of whole body passive hyperthermia increases plasma leptin, but does not alter glucose or insulin responses in obese type 2 diabetics and healthy adults.
Acute and chronic hyperthermic treatments in diabetic animal models repeatedly improve insulin sensitivity and glycemic control. Therefore, the purpose of this study was to test the hypothesis that an acute 1h bout of hyperthermic treatment improves glucose, insulin, and leptin responses to an oral glucose challenge (OGTT) in obese type 2 diabetics and healthy humans. Nine obese (45±7.1% fat mass) type 2 diabetics (T2DM: 50.1±12y, 7.5±1.8% HbA1c) absent of insulin therapy and nine similar aged (41.1±13.7y) healthy non-obese controls (HC: 33.4±7.8% fat mass, P<0.01; 5.3±0.4% HbA1c, P<0.01) participated. Using a randomized design, subjects underwent either a whole body passive hyperthermia treatment via head-out hot water immersion (1h resting in 39.4±0.4°C water) that increased internal temperature above baseline by ∆1.6±0.4°C or a control resting condition. Twenty-four hours post treatments, a 75g OGTT was administered to evaluate changes in plasma glucose, insulin, C-peptide, and leptin concentrations. Hyperthermia itself did not alter area under the curve for plasma glucose, insulin, or C-peptide during the OGTT in either group. Fasting absolute and normalized (kg·fat mass) plasma leptin was significantly increased (P<0.01) only after the hyperthermic exposure by 17% in T2DM and 24% in HC groups (P<0.001) when compared to the control condition. These data indicate that an acute hyperthermic treatment does not improve glucose tolerance 24h post treatment in moderate metabolic controlled obese T2DM or HC individuals.
Institute for Clinical and Translational Science & Department of Pediatrics, The University of California, Irvine, CA, USA; Department of Kinesiology, Texas Woman's University, Denton, TX, USA; Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, TX, USA and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: erivas4@uci.edu.
Eric
E
Rivas
Department of Kinesiology, Texas Woman's University, Denton, TX, USA.
Dan E
DE
Newmire
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, TX, USA and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Craig G
CG
Crandall
Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Philip L
PL
Hooper
Department of Kinesiology, Texas Woman's University, Denton, TX, USA.
Vic
V
Ben-Ezra
D000328:Adult; D001786:Blood Glucose / Q000032:analysis* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D006979:Hyperthermia, Induced / Q000379:methods*; D007328:Insulin / Q000097:blood* / Q000378:metabolism; D020738:Leptin / Q000097:blood* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications
D001786:Blood Glucose; D007328:Insulin; D020738:Leptin
Diabetes; Glycemic control; Hyperthermia; Leptin; Obesity; Thermal stress