Degree of weight loss required to improve adipokine concentrations and decrease fat cell size in severely obese women Krista A. Varady ⁎ , Lisa Tussing, Surabhi Bhutani, Carol L. Braunschweig Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL 60612, USA Received 13 February 2009; accepted 8 April 2009 Abstract Adipose tissue physiology plays an important role in mediating disease risk. Weight loss in obese individuals improves indicators of adipocyte physiology. However, the minimum degree of weight loss required to elicit improvements remains unknown. The objective of the present study was to determine the minimum weight loss required to improve adipokine profile and decrease fat cell size in severely obese women. Thirteen severely obese women (body mass index, 50 ± 3 kg/m 2 ; age, 35 ± 1 years) consumed a low-calorie diet for 3 weeks with the goal of losing 5% of their initial weight. Subjects were divided into 2 weight loss groups posttreatment: less than 5% weight loss and 5% to 10% weight loss. Body weight was reduced (P b .05) in both groups (-1.4 ± 1.0 and -6.8 ± 0.6 kg, respectively). Adiponectin concentrations increased (P b .05) by 20% in the 5% to 10% weight loss group only. Likewise, leptin and resistin decreased (P b .05) by 37% and 27%, respectively, in the group that lost more weight. Visceral and subcutaneous fat cell size was 41% and 37% smaller (P b .01), respectively, in the 5% to 10% weight loss group. Smaller visceral adipocyte size was related to lower insulin (r = 0.82, P = .01) and glucose (r = 0.58, P = .04) concentrations posttreatment. These findings suggest that a minimum weight loss of 5% is required to improve adipokine profile and decrease fat cell size in severely obese women. These changes in adipocyte physiology may be linked to reductions in metabolic disease risk in this population. © 2009 Elsevier Inc. All rights reserved. 1. Introduction Excess fat content in adipose tissue is strongly associated with the development of several obesity disorders including coronary heart disease (CHD) and type 2 diabetes mellitus [1]. Although the mechanisms underlying these obesity- related disorders remain unclear, recent evidence suggests that adipose tissue physiology (ie, fat cell–derived hormones and fat cell size) may provide a link between obesity and disease risk [1,2]. To date, more than 25 fat cell–derived hormones (ie, adipokines) have been discovered. Of these, adiponectin, leptin, and resistin have received considerable attention. Adiponectin exerts both insulin-sensitizing and antiatherogenic effects, and circulating levels of this beneficial adipokine increase with weight loss [3]. Leptin, in contrast, exhibits proatherogenic and proinflammatory properties; and concentrations of this hormone decrease as body weight declines [4]. Resistin, like leptin, has been implicated in the pathogenesis of insulin resistance and atherosclerosis, and is reduced when body mass decreases [5]. Circulating levels of these hormones are, in part, dictated by fat cell size. Obese individuals have larger visceral and subcutaneous fat cells when compared with their normal- weight counterparts [2]. Larger adipocytes release higher amounts of the proinflammatory mediators leptin and resistin, and lower amounts of the anti-inflammatory adi- pokine adiponectin [2]. As an individual loses weight, concomitant decreases in fat cell size are often observed [2]. Findings from the 2007 Behavioral Risk Factor Surveil- lance System survey estimate that 3 of every 100 women in the 20- to 39-year–old age group are severely obese (body mass index [BMI] N35 kg/m 2 ) [6]. Carrying extra weight puts these women at increased risk for both CHD and type 2 diabetes mellitus. Losing weight, even a relatively small amount of weight, has been shown to improve metabolic disease risk indicators, such as insulin, glucose, and C- reactive protein (CRP) concentrations [7]. Small decreases in body weight also reduce fat cell size [8] and improve Available online at www.sciencedirect.com Metabolism Clinical and Experimental 58 (2009) 1096 – 1101 www.metabolismjournal.com ⁎ Corresponding author. Tel.: +1 312 996 7897; fax: +1 312 413 0319. E-mail address: varady@uic.edu (K.A. Varady). 0026-0495/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.metabol.2009.04.010