Nutrition and Health Sciences, Department of

 

First Advisor

Karsten Koehler

Date of this Version

7-2017

Citation

A. R. Martin, Adaptive Thermogenesis and Metabolic Changes Following Diet- and Exercise- Induced Weight Loss, UNL Digital Commons, 2017.

Comments

A THESIS Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Master of Science, Major: Nutrition and Health Sciences, Under the Supervision of Professor Karsten Koehler. Lincoln, Nebraska: July 2017

Copyright (c) 2017 Alexandra R. Martin

Abstract

With more than two-thirds of adults in the United States considered as overweight or obese, a myriad of weight loss programs and products that promise quick results have infiltrated the market. While many individuals successfully lose weight over the short term, almost half of the initial weight lost is regained within one year, indicating a general predisposition for weight cycling and fat replenishment. As weight is lost, fat-free mass (FFM) also decreases, and resting metabolic rate (RMR) declines, decreasing energy expenditure. After accounting for decreases in FFM, there remains a greater-than- predicted decrease in RMR, referred to as adaptive thermogenesis (AT), which describes the suppression of non-vital functions to re-equilibrate energy status. The overall goal of this thesis is to quantify adaptive thermogenesis and determine the role of suppressed brown adipose tissue (BAT) activity in this adaptive response. An exploratory study in normal weight participants revealed a 5.4% increase in RMR following mild cold exposure as well as prominent increases in surface supraclavicular temperature, a region that indicate the presence of cold-induced thermogenesis (CIT) of BAT. Study 1 demonstrated that overweight/obese participants had a significantly greater RMR (p=0.04) and concentrations of leptin, insulin, and FGF-21 (p=0.015, p=0.091, p=0.023) than normal weight participants, but no significant difference in adaptive thermogenesis (220 ± 40 kcal vs. 89 ± 15 kcal, p=0.20) or surface body temperatures were found. Study 2 revealed a reduction in RMR by 209 ± 1 kcal in normal-weight individuals undergoing severe calorie restriction, which was associated with reductions in insulin (-23.9 ±14.8 pg/mL) and FGF-21 (-61.6 ± 28.7 pg/mL). In study 3, there were no significant changes in RMR, AT, or metabolic hormones over the course of a 3-month commercial weight loss intervention, which failed to produce significant weight loss. Indications of adaptive thermogenesis were present in both normal weight and obese/overweight participants, though AT was more pronounced in the latter. With the link between adaptive thermogenesis and modulation of BAT activity, cold exposure and brown fat activation may be an effective tool to increase energy expenditure during a period in which RMR is suppressed, thus preventing future weight regain.

Advisor: Karsten Koehler

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