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Got Fat? Pass the Testosterone Please!
by: Tom Rayhawk

Consider this: how many times have you read or heard that there is no such thing as a “cutting” steroid? For years the generally accepted doctrine was that steroids do not reduce adipose tissue but rather can decrease water retention and inhibit estrogen’s actions thus producing the “hard” look. Furthermore, the consensus seems to be that while testosterone and related anabolic substances certainly aid the dieting bodybuilder it is only via the androgen’s anti-proteolytic abilities, thus sparing muscle tissue while in a hypocaloric state, in addition to the aforementioned “drying out” effect.

In short – this is hogwash!! As this article will validate, an abundance of clinical research and peer-reviewed data strongly supports testosterone’s (T) fat reducing actions and its preventative impact on adipocyte generation (1,2,3). Therefore, T acts both in the breakdown of existing fat tissue and to hinder pre-adipocytes from maturing. CCAAT enhancer-binding proteins (CEBPs) are vital contributors at several stages of adipogenesis – or fat cell formation – from early uptake and accumulation of lipids to the differentiation, proliferation, and terminal production of the adipocyte. CEBPs exist in an alpha, sigma, and beta form. The beta and sigma form promote the transcription of PPARy2, which is arguably the most important factor in fat cell formation. CEBP possesses intrinsic pro-adipogenic activity independent of PPARy2. Specifically, the alpha and sigma isoform of CEBP interact with promoter regions of DNA involved in adipose development (5). PPARy2, stimulated by the CEBP isoforms, is capable of the same. This leads to a viscous cycle beginning with CEBP activity. DNA promotion of said adipogenic proteins follows, including PPARy2, which itself then activates the same lipid-related genes as the CCAAT enhancer-binding proteins. Testosterone has been shown to reduce all three forms of CEBP’s, which, predictably, curtails PPARy2 functions (5, 6, 7, 17, 23). Evidence exists as well that dihydrotestosterone shares T’s anti-CEBP characteristics (6, 23). Like muscle tissue, fat cells express anabolic receptors, which bind to respective androgens and initiate inhibitory effects on CEBP’s. Visceral Adipose Tissue (VAT) is more sensitive to T than subcutaneous fat (SC). This is most likely explained by the fact that AR’s occur in greater number in VAT versus SC tissue (2, 3, 4). T’s strong effect on VAT coincides with the observed reduction in abdominal fat in hypogonadal men placed on testosterone therapy. Furthermore, T’s antiadiogenic and lipolytic actions are more predominant in VAT (1, 2). Pre-adipocytes, located in VAT, show reduced activity of the CEBP’s when exposed to testosterone (5, 6). A novel observational study followed 511 males aged 30-79, over a 12-year period charting the effects of serum androstenedione, testosterone, and SHBG and their relation to VAT. Hormone analysis was conducted before and after this period and concluded that below normal androstenedione and testosterone show strong correlation with abdominal adipose tissue. (8). Peroxisomal proliferator-activated receptor gamma 2 is another protein that functions to increase the differentiation of adipocytes. Treatment with either testosterone or DHT reduces PPARg2 providing another means whereby androgens discourage the differentiation stage in adipogenesis (22) The metabolic alterations experienced in VAT due to testosterone are of significance with both negative and positive ramifications. Lipid uptake is inhibited in VAT mainly due to a decrease in lipoprotein-lipase activity, and a reduction in serum insulin and glucose levels (9). It should be noted that lipid uptake is enhanced by elevated hyperglycemia/hyperinsulinemia, primarily in VAT (10). So the decrease in VAT noted with a reduction of glucose/insulin levels – via testosterone elevation – should make sense. The ability of testosterone to stimulate fatty acid release from VAT can be problematic, though. Feeding directly into the liver via the portal vein, these fatty acids have the potential to impair both insulin sensitivity and function, induce hyperglycemia, and increase LDL levels. Ultimately this can lead to hyperinsulinemia, hyperglycemia, hyperlipidemia, and hypertension, vascular resistance, all of which are consistent with the pathology of “Metabolic Syndrome X” (11). In addition, cortisol, originating in VAT, is also released and fed to the liver via the portal vein. This exacerbates fat cell maturity as cortisol increases the differentiation of pre-adipocytes into the adult forms (13). It would seem logical then to suggest a cause and effect relationship between free fatty acid release from VAT by testosterone and the development the conditions of Metabolic Syndrome X. This may be a moot point though as testosterone treatment has been associated with an actual reduction in both total cholesterol and LDL levels. Previous studies indicate that testosterone – especially its chemically altered versions – can lower HDL levels deemed the “good cholesterol”. This has not been demonstrated conclusively, as results of other research efforts imply that T is neutral in regards to HDL, neither causing a significant increase or decrease (12, 16). In relation to the cardiovascular disorders, normal or slightly enhanced T levels might exert a protective effect. Pro-inflammatory cytokines TNF , IL-1ß, and IL-6 in human macrophages, are positively associated with congestive heart failure and atherosclerosis. Not only has testosterone been shown to reduce the elevations in these cytokines but also up regulates anti-inflammatory cytokines such as IL-10, leading to an improvement in improving overall cardiovascular function. (12, 14, 15) This decreases susceptibility to congestive heart failure and vascular disease also due in part to T’s vasodilating characteristics.

In relation to existing fat tissue, T levels are inversely associated with lipoprotein lipase, an enzyme involved in the breakdown of triglycerides and recycling of the resulting fatty acids and eventual production a mature lipid-rich adipocyte. Testosterone also impairs overall lipid uptake into fat cells, hindering hypertrophy of existing fat cells. T is positively correlated with beta receptor number catecholamine sensitivity, thus heightening thermogenesis (18, 19, 20). The thermogenic process involves a G-protein activation and a downstream production of lipolytic enzymes and proteins. Both DHT and Testosterone amplifies adenylate cyclase activity, an enzyme vital to beta receptor stimulated lipolysis (21). Moreover, hormone-sensitive lipase (HSL) initiates the breakdown of stored tryiglycerides into fatty acids, which can be oxidized and thus “burned” in either mitotochondria and/or peroxisomes. T not only elevates HSL but also Protein Kinase A, an enzyme that functions in the G-protein stimulated lipolysis (18, 20) By jacking up these lipolytic enzymes and proteins, beta oxidation occurs. Androgens also increase other such enzymes including carboxylesterase 3, acetyl-coenzyme A acyltransferase 1, 3-ketoacyl-CoA thiolase B and enoyl-coenzyme A hydratase/3-hydroxyacyl coenzyme A dehydrogenase (2, 24). Enzymes vital to lipogenesis, conversely, show a consistent negative correlation with both T and DHT. Malic enzyme, glyceraldehyde dehydrogenase (GDH), and fatty acid elongation factors – all capable of pro-lipogenic effects, are inhibited by DHT and T (2, 24) It is of great importance, though, to understand that the T’s positive benefits espoused in this article DO NOT apply to females. In fact, typically, the majority of natural male androgens, such as testosterone and DHT, exert converse or opposing actions – often negative – in females compared to males. Furthermore, the studies and research cited herein refer to inherent activity of endogenous T and DHT or hormone replacement therapy (HRT). These intrinsic natural androgens and their actions, thus, do not extend to chemical altered androgens or anabolic steroids. This does not necessarily imply that AAS do not have the potential to mimic endogenous male hormone. This just indicates that only research reviews examining naturally produced androgens were considered herein. If truth be told, a follow-up article delving even deeper into functions of T on obesity would certainly be justified. It also could review effects of both testosterone in females and chemically altered androgens. This article provides a fairly brief review of what is actually an impressive and growing body of evidence supporting Testosterone and other androgens as potent lipolytic and anti-adipogenic hormones. In fact, while the author had reviewed relevant literature beforehand describing the interactions of androgens and adipose, the additional dissection of this topic revealed a much greater than anticipated number of mechanisms and actions of natural androgens. Testosterone has not really received the respect and appreciation it deserves for its wide range of health benefits. Recently, though, with the ever-increasing administration of HRT to males and evidence confirming its potential benefits, the negative connotation and exaggerated drawbacks of such treatment is dying out. In its place exists a wealth of legitimate research claims and an increased priority placed on unbiased future studies.


1.Peter J. Snyder, Helen Peachey, Peter Hannoush, Jesse A. Berlin, Louise Loh, David A. Lenrow, John H. Holmes, Abdallah Dlewati, Jill Santanna, Clifford J. Rosen and Brian L. Strom. Effect of Testosterone Treatment on Body Composition and Muscle Strength in Men Over 65 Years of Age1The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 8 2647- \

2.Hutley L, Joyner J Cameron D. Intrinsic Horm Metab Res. 2002 May;34(5):223- regional differences in androgen receptors and dihydrotestosterone metabolism in human preadipocyte. 3. M. N. Dieudonné, R. Pecquery, A. Boumediene, M. C. Leneveu, and Y. Giudicelli. Androgen receptors in human preadipocytes and adipocytes: regional specificities and regulation by sex steroids Am J Physiol Cell Physiol 274: C1645-C1652, 1998; 4 Androgen hormone binding to adipose tissue in rats. Sjogren J, • Li M, • Bjorntorp P. Biochim Biophys Acta. 1995 May 11;1244(1):117–120 5 Rajan Singh, Jorge N. Artaza, Wayne E. Taylor, Melissa Braga, Xin Yuan, Nestor F. Gonzalez-Cadavid and Shalender Bhasin Testosterone Inhibits Adipogenic Differentiation in 3T3-L1 Cells: Nuclear Translocation of Androgen Receptor Complex with ß-Catenin and T-Cell Factor 4 May Bypass Canonical Wnt Signaling to Down-Regulate Adipogenic Transcription Factors. Endocrinology Vol. 147, No. 1 141-154 6. Rajan Singh, Jorge N. Artaza, Wayne E. Taylor, Nestor F. Gonzalez-Cadavid and Shalender Bhasin. Androgens Stimulate Myogenic Differentiation and Inhibit Adipogenesis in C3H 10T1/2 Pluripotent Cells through an Androgen Receptor-Mediated Pathway. Endocrinology, doi:10.1210/en.2003-0741 7. Shalender Bhasin, Thomas W. Storer, Nancy Berman, Kevin E. Yarasheski, Brenda Clevenger, Jeffrey Phillips, W. Paul Lee, Thomas J. Bunnell and Richard Casaburi. Testosterone Replacement Increases Fat-Free Mass and Muscle Size in Hypogonadal Men1. The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 2 407-413 8. Khaw KT, Barrett-Connor E. Lower endogenous androgens predict central adiposity in men. Horm Metab Res. 2002 May;34(5):223-8 9. P Marin, B Oden and P Bjorntorp Assimilation and mobilization of triglycerides in subcutaneous abdominal and femoral adipose tissue in vivo in men: effects of androgens. Journal of Clinical Endocrinology & Metabolism, Vol 80, 239-243, 10. Marin P, Andersson B, Ottosson M, Olbe L, Chowdhury B, Kvist H, Holm G, Sjostrom L, Bjorntorp P. The morphology and metabolism of intraabdominal adipose tissue in men. Metabolism. 1992 Nov;41(11):1242-8. 11. Bergman RN, Kim SP, Hsu IR, Catalano KJ, Chiu JD, Kabir M, Richey JM, Ader M. Abdominal obesity: role in the pathophysiology of metabolic disease and cardiovascular risk. Am J Med. 2007 Feb;120(2 Suppl 1):S3-8; discussion S29-32. 12. Chris J. Malkin, Peter J. Pugh, Richard D. Jones, Dheeraj Kapoor, Kevin S. Channer and T. Hugh Jones. The Effect of Testosterone Replacement on Endogenous Inflammatory Cytokines and Lipid Profiles in Hypogonadal Men. The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 7 3313-3318 13. Ruth Andrew1, Jukka Westerbacka2, John Wahren3, Hannele Yki-Järvinen2, and Brian R. Walker1. The Contribution of Visceral Adipose Tissue to Splanchnic Cortisol Production in Healthy Humans. Diabetes 54:1364-1370, 2005 14. Cutolo M, Balleari E, Giusti M, Intra E, Accardo S. Androgen replacement therapy in male patients with rheumatoid arthritis. Arthritis Rheum. 1991 Jan;34(1):1-5. 15. P J Pugh1, R D Jones2, J N West1, T H Jones2 and K S Channer1. Testosterone treatment for men with chronic heart failure. Heart 2004;90:446-447 16. D Kapoor1,3, E Goodwin1, K S Channer2 and T H Jones1,3. Testosterone replacement therapy improves insulin resistance, glycemic control, visceral adiposity and hypercholesterolaemia in hypogonadal men with type 2 diabetes. European Journal of Endocrinology, Vol 154, Issue 6, 899-906 17. E Garcia, M Lacasa, B Agli, Y Giudicelli, and D Lacasa. Modulation of rat preadipocyte adipose conversion by androgenic status: involvement of C/EBPs transcription factors. Journal of Endocrinology, Vol 161, Issue 1, 89-97 18. XF Xu, G De Pergola and P Bjorntorp. Testosterone increases lipolysis and the number of beta-adrenoceptors in male rat adipocytes. Endocrinology, Vol 128, 379-382, 19. Rebuffé-Scrive M, Mårin P, Björntorp P. Effect of testosterone on abdominal adipose tissue in men. Int J Obes. 1991 Nov;15(11):791-5. 20. X Xu, G De Pergola, PS Eriksson, L Fu, B Carlsson, S Yang, S Eden and P Bjorntorp. Postreceptor events involved in the up-regulation of beta-adrenergic receptor mediated lipolysis by testosterone in rat white adipocytes. Endocrinology, Vol 132, 1651-1657 21. Pecquery R, Dieudonne MN, Leneveu MC, Giudicelli Y. Evidence that testosterone modulates in vivo the adenylate cyclase activity in fat cells. Endocrinology. 1990 Jan;126(1):241-5 22. Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, Bhasin S. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology. 2003 Nov;144(11):5081-8. Epub 2003 Jul 24. 23. M. N. Dieudonne, R. Pecquery, M. C. Leneveu and Y. Giudicelli. Opposite Effects of Androgens and Estrogens on Adipogenesis in Rat Preadipocytes: Evidence for Sex and Site-Related Specificities and Possible Involvement of Insulin-Like Growth Factor 1 Receptor and Peroxisome Proliferator-Activated Receptor 2. Endocrinology Vol. 141, No. 2 649-656 24. Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Opposite effects of androgens and estrogens on adipogenesis in rat preadipocytes: evidence for sex and site-related specificities and possible involvement of insulin-like growth factor 1 receptor and peroxisome proliferator-activated receptor gamma2. Endocrinology. 2000 Feb;141(2):649-56.

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