Regional changes in adrenergic receptor status during hypocaloric intake do not predict changes in adipocyte size or body shape

Abstract

The anatomic distribution of fat is related to the risk for obesity-associated morbidity. Among individuals with equal degrees of relative adiposity, those with an upper-body preponderance of fat distribution (android) have higher rates of diabetes, stroke, ischemic heart disease, and early death than those with preferential deposition of adipose tissue in lower portions of the body (hips, thighs, buttocks; gynecoid. There are well-documented anatomic site-related differences in the relative activities of the adrenergic receptors ( β 1 → lipolysis; α 2 → antilipolysis) that control lipolysis. We assessed modifications of the status of α 2- and β 1-adrenergic receptor and subreceptor function in small fragments of adipose tissue obtained by needle biopsy from the gluteal and abdominal subcutaneous regions of five android, seven gynecoid, and six uniformly obese women during a period of weight maintenance (4 weeks) (T1), and after 15% weight loss on an 840 kcal/d diet (T2). Measurements of body shape and adipocyte size were made and related to changes in the metabolism of these adipocytes. The waist-to-hip ratio (WHR) was used to define these three types of regional distribution of fat in these obese subjects: android = WHR >0.86; gynecoid = WHR ≤ 0.76; uniform = WHR > 0.76 ≤ 0.86. WHR was not significantly altered by weight loss in any of the three groups. Although significant effects of time and/or anatomic site on in vitro responses to isoproterenol, norepinephrine, clonidine, forskolin, and dibutyryl cAMP were found, these did not correlate with intra-individual changes in anthropometry or adipocyte size. Thus, the mobilization of lipid from specific subcutaneous anatomic sites during long-term restriction of caloric intake does not appear to be related to alterations in the functional status of the adrenergic receptor or subreceptor mechanisms studied. The precise mechanisms by which the body regulates fat mobilization under these circumstances remain unknown.