那是个很有趣的难题。绝大大都女性健身活动者关于激素的知觉次要就在雌化、蓄水池、介导性激素等方面。
固然也依稀晓得女性需要一些激素，但是绝大大都女性健身活动者一般仍是认为女性要尽量制止激素水准。
其实激素对女性的促进感化良多，好比避免营养不良和为庇护肌肉。在中文互联网上，我还没有见过谁详细的写过阿谁话题，我们今天就专门讲下。
一、激素有助于避免女性营养不良营养不良是一种全球性的疾病，是一个愈来愈严峻的卫生保健难题。全球埃唐佩县和营养不良生齿超越20亿，所以阿谁数字还在不竭增加[1] [2] [3]。留意，营养不良与DNA有很大的关系[4] [5] [6]，也跟激素有关。
人类是近20年才晓得激素能为庇护女性、削减营养不良的。2006年，Jones等人初次辨认出并报导，女性若是贫乏激素，会引致营养不良[7]。
不成承认，女性胃部的激素次要就源自子宫，而女性胃部的激素仅有约15%源自阴茎[8]，而大部门次要就源自香气酶。香气酶次要就存在于结缔组织中，负责将雌激素转化为激素。
若是香气酶的数目或者机能不恒定，女性就无法获得足够的激素。Jones等人辨认出7名女性即便呈现了CYP19DNA的内含子变异，引致她们胃部的香气酶机能障碍，因而它胃部的激素水准低得几乎检测不到，所以她们的性激素水准中低偏高。
图1『激素水准较低、雌激素水准中低略高』，良多男网友可能觉得那是功德，即便她们都传闻了『激素过多引致女性乳房生长发育、极化、营养不良』的说法。
然而，胃部激素水准较低的那7名女性头上有一次病，比骨骼生长发育迟滞、骨量酥松、营养不良、生长激素抵御，还有广阔FANS最不想呈现的：生殖机能降低。
为了验证阿谁难题能否偶尔，Jones等人进一步的检视，辨认出香气酶DNA卢瓦龙县的雌性大鼠头上也检视到了类似的情况；通过那些检视她们证明，激素在调理哺乳鸟类的体重、营养不良和乳酸胃部平衡中，阐扬了决定性的为庇护促进感化。
以至有些科学研究认为，雌性鸟类『贫乏激素』可能比『贫乏雌激素』更差劲[9]，『贫乏激素』可引致雌性鸟类的埃唐佩县比其他恒定雌性鸟类翻番[10] [11]。
Heine等他用DNA卢瓦龙县手艺造造了雌激素卵白卢瓦龙县的雌性大鼠[12]（KO大鼠），那些大鼠胃部能形成雌激素，但它大部分的细胞上都没有激素卵白，相当于隐性失去了大部分激素。
KO雌性大鼠随年龄增长胃部的白色结缔组织愈来愈多，到270-360Acheilognathus时，与恒定大鼠比拟，KO大鼠的输尿管、肾脏四周和尿道的碳水化合物细胞增大20%、碳水化合物细胞数目激增82-168%、结缔组织重量激增139%-185%。
图2：30和90Acheilognathus三组大鼠碳水化合物量对照图3：180和270-360Acheilognathus三组大鼠碳水化合物量对照值得一提的是，该科学研究中的通俗雌性大鼠和KO雌性大鼠摄取的热能是那样的。那句话让会让良多瘦身只考虑总热能的人胸口痒，即便她们始末都是错的，她们始末认为瘦身地道就是吃和运动的的难题，就地道只是总热能的难题。
图4那是一个驳倒『高矮只看总热能』的典型证据，在摄取热能那样的情况下，KO雌性大鼠比恒定雌性大鼠胖多了（图4）。
它摄取热能不异但却胖的多的原因不完全清晰，但科学研究者认为是ko雌性大鼠日常消耗的热能更少，大约少了11%（以及肌肉量削减）。
让雌性大鼠失去激素信号，除了卢瓦龙县它的激素卵白DNA，还能够卢瓦龙县她们的香气酶DNA，即便雌性哺乳鸟类的大部门激素源自于碳水化合物细胞内的香气酶。
碳水化合物细胞内的Cyp19DNA编码出香气酶，只要毁坏了阿谁DNA，大鼠就不克不及形成香气酶[13]；Jones等人操纵那种体例获得了香气酶卢瓦龙县大鼠（ArKO）[14]，它根本不克不及合成内源性激素。
成果跟Heine等人[12]的科学研究彼此撑持，香气酶卢瓦龙县的大鼠（ArKO大鼠），不管雌性仍是雌性，都变得更胖了。在1岁的年龄下，关于肾脏四周的碳水化合物积累（图5），ArKO雌性大鼠均匀213.2g，通俗大鼠均匀105.8g，差距几乎一倍；
图5性腺四周的碳水化合物细胞大小（图6），也是ArKO大鼠（B）明显比通俗大鼠（A）更大；
图6在全身碳水化合物总量方面（图7），ArKO大鼠（黑柱）明显比通俗大鼠（白柱）更多，不管雌性和雌性都是如斯；而且雌性ArKO大鼠的营养不良似乎比雌性更严峻。
图7关于肝脏的碳水化合物堆积（图8），ArKO大鼠明显比通俗大鼠更严峻；下图是对那些大鼠尸检的肝脏切片，肝细胞自己是恩红色，此中白色部门就是肝脏的碳水化合物堆积。
图8关于ArKO大鼠营养不良的原因，做者强调：
excess body fat in the estrogen-insufficient ArKO mice was not due to hyperphagia or reduced resting energy expenditure, but was associated with decreased lean mass and reduced spontaneous physical activity.
激素不敷的ArKO大鼠胃部多余的碳水化合物，不是因为摄食过量引致的，而是即便瘦体重（肌肉组织削减）、静息能量消耗减低、身体活动削减形成的。
二、激素通过中枢神经调理体重和能量代谢文献表白，激素信号通过通过中枢神经机造[15] [16]。
下丘脑是食欲和能量消耗以及生殖行为的次要就调理部位[17] [18]，下丘脑也有丰硕的激素卵白，出格是在弓状核、室旁核和腹内侧核[15] [19] [20]；所以，中枢神经系统中，如星型胶量细胞和神经元，具有将胆固醇合成激素所必需的酶[21]。
有趣的是，给雌性大鼠喂食大量的动物激素，虽然它的食欲增加，但营养不良率却下降了[22]。
那可能是即便激素信号影响了下丘脑，好比Ogawa等人检视到切除阴茎后打针激素的雌性大鼠自主日常活动增加[23]（跑滚轮）——那与Heine等人[12]陈述说激素不敷的雌性大鼠瘦体重和身体活动削减相吻合。
三、激素维持胰岛敏感性，为庇护骨骼肌几乎大部分人都晓得雌激素（性激素类）对骨骼肌的重要为庇护促进感化。但是少少有网友晓得激素也对肌肉具有为庇护促进感化，上面的良多科学研究中都提到了那一点。
起首是Jones等人[7]报导激素在调理哺乳鸟类的葡萄代谢中阐扬了决定性的为庇护促进感化，然后Heine等他用DNA卢瓦龙县手艺造造的雌激素卵白卢瓦龙县的雌性大鼠[12]（KO大鼠）的血糖和血液生长激素水准更高（图9）。
图9消化过程中，食物（碳水化合物）从小肠以乳酸的形式吸收入血，再在生长激素[24] [25]的帮忙下进入各器官；生长激素从血液抵达肌细胞外表后[26]与卵白连系[27] [28] [29] [30]，引发一系列细胞内的生物化学信号[31] [32]，促使乳酸转运卵白往细胞外表挪动，细胞摄取乳酸。
图10若是骨骼肌呈现了胰岛抵御，血糖无法顺利进入骨骼肌，就会滞留在血液中，引起血糖升高；同时，身体味排泄更多的生长激从来促进血糖进入骨骼肌（和其他器官）。所以血糖和血浆生长激素都升高，就是胰岛抵御的标记。
生长激素的促进感化对增肌来说十分重要。
抗阻训练后的肌肉增长具有生长激素依赖性；有足够生长激素时，卵白合成速度显著增加[33]；利用按捺生长激素排泄的药物后，大鼠比目鱼肌、腓肠肌和肋上肌的卵白量合成明显削减[34]；利用抗生长激素抗体消弭了生长激素的促进感化，几乎完全阻断了氨基酸对肌肉卵白量合成的刺激[35]；生长激素还能与氨基酸协同促进感化，形成1+1＞2的效果，放大卵白量合成的效率[36] [37]；生长激素通过刺激一氧化氮合成来扩张毛细血管[38]，肌细胞得到更多的血流量[39] [40] [41]和营养物量；生长激素抵御则意味着肌细胞摄取的营养削减[42] [43] [44] [45]；2型肌纤维做为人体增肌的主力[46]，它以糖酵解为次要就能量[46]。有些新同窗可能会问，肌肉的胰岛敏感性降低，肌肉获得的糖削减，肌肉能不克不及以碳水化合物做为能量来源呢？
阿谁难题我们解答过，碳水化合物其实不能零丁氧化供能，它需要糖类衍生物（草酰乙酸）的共同，才气氧化供能。若是乳酸削减，又能量匮乏，人体就只能氧化卵白量来获得所需的草酰乙酸[47] [48]。
碳水化合物燃烧需要碳水吗?915 附和 · 65 评论答复那就是为什么糖尿病人、或者胰岛抵御的鸟类，城市呈现显著的骨骼肌流失。严峻糖尿病大鼠中，骨骼肌卵白量合成明显削减[49] [50] [51]；若是利用药物诱导大鼠糖尿病，大鼠空腹血浆生长激素浓度降低到对照组安康大鼠的25%，糖尿病大鼠腓肠肌的卵白量合成水准也是对照大鼠的25%[52]。
胰岛抵御是肌肉杀手。
胰岛抵御是肌肉杀手。
胰岛抵御是肌肉杀手。
重要的事说三通。
回到本文，激素对女性（和女性）来说，具有维持胰岛敏感性、为庇护骨骼肌的促进感化，那解释了为什么绝经前的女性糖尿病发病率低于女性[53] [54]。
做为对照，喂食高碳水化合物饮食引致雌性鸟类的胰岛敏感性降低40-50%[55] [56]，但雌性鸟类和人类女性受益于激素的代谢为庇护促进感化，胰岛抵御水平较少[57] [58] [59] [60]；在医学上也检视到，子宫切除会损害肌肉乳酸摄取和贮存，会引致肌肉削减[61] [62]。
激素对胰岛敏感性和肌肉的为庇护机造很复杂，所以是多样化的：
激素诱导AMPK激活[63] [64]；激素维持乳酸转运卵白数目[65]（Glut4）；激素促进Glut4在运动后数目上调[66] [67]；激素激活肌肉合成代谢信号（Akt信号）[68] [69] [70]；激素通过FOXO1按捺肌肉合成的酶（泛素毗连酶）[71]。那些内容比力深，我们在本文就不铺开说了。
有趣的是，激素对女性（和女性）埃唐佩县的控造促进感化和肌肉的为庇护促进感化，可能解释了为什么女性热衷于瘦身。激素关于女性营养不良具有按捺促进感化：失去激素的为庇护，雌性鸟类和人类绝经后，胰岛敏感性急剧下降、埃唐佩县和炎症水准增加[72] [73]。
所以，也许从潜意识里，女性对瘦的逃求，其实是一种潜意识里对青春（激素控造埃唐佩县）的逃求，或者说是挽留；她们希望通过运动瘦身，把本身酿成年轻时有丰硕激素水准的苗条形态。
扩展阅读肉崽：生长激素到底可以增加肌纤维数目吗？
肉崽：有哪些容易引致人体小腹容易堆积碳水化合物的，具有普适性的原因？
肉崽：碳水化合物在运动过程中是怎么改变为能量的，人体消耗的碳水化合物是不是有位置优先级？
肉崽：为什么都说增肌要碳水？
肉崽：埃唐佩县高能否影响增肌?
肉崽：为什么牛吃草就能长肌肉，人却要吃卵白量而且还要不断熬炼？
参考^ Organization WH. Obesity: preventing and managing the global epidemic. 2000^Van Vliet-Ostaptchouk JV, Snieder H, Lagou V. Gene–lifestyle interactions in obesity. Curr Nutr Rep. 2012;1(3):184–96. ^Reddon H, Gerstein HC, Engert JC, Mohan V, Bosch J, Desai D, et al. Physical activity and genetic predisposition to obesity in a multiethnic longitudinal study. Sci Rep. 2016;6(1):1–10.^ Albuquerque D, Manco L, Nóbrega C. Genetics of human obesity. Obesity: Springer; 2016. pp. 87–106.^Montague CT, Farooqi IS, Whitehead JP, Soos MA, Rau H, Wareham NJ, et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature. 1997;387(6636):903–8. ^ Albuquerque D, Nóbrega C, Manco L, Padez C. The contribution of genetics and environment to obesity. Br Med Bull. 2017;123(1):159–73. ^abJones ME, Boon WC, Proietto J, Simpson ER. Of mice and men: the evolving phenotype of aromatase deficiency. Trends Endocrinol Metab. 2006;17:55–64. ^Hemsell DL, Grodin JM, Brenner PF, Siiteri PK, MacDonald PC. Plasma precursors of estrogen. II. Correlation of the extent of conversion of plasma androstenedione to estrone with age. J Clin Endocrinol Metab. 1974;38:476–479. ^Fan W, Yanase T, Nomura M, Okabe T, Goto K, Sato T, Kawano H, Kato S, Nawata H. Androgen receptor null male mice develop late-onset obesity caused by decreased energy expenditure and lipolytic activity but show normal insulin sensitivity with high adiponectin secretion. Diabetes. 2005;54:1000–1008. ^Cooke PS, Heine PA, Taylor JA, Lubahn DB. The role of estrogen and estrogen receptor-alpha in male adipose tissue. Mol Cell Endocrinol. 2001;178:147–154.^Ohlsson C, Hellberg N, Parini P, Vidal O, Bohlooly-Y M, Bohlooly M, Rudling M, Lindberg MK, Warner M, Angelin B, Gustafsson JA. Obesity and disturbed lipoprotein profile in estrogen receptor-alpha-deficient male mice. Biochem Biophys Res Commun. 2000;278:640–645.^abcdHeine PA, Taylor JA, Iwamoto GA, Lubahn DB, Cooke PS. Increased adipose tissue in male and female estrogen receptor-alpha knockout mice. Proc Natl Acad Sci U S A. 2000;97:12729–12734.^Fisher C R, Graves K H, Parlow A F, Simpson E R. Proc Natl Acad Sci USA. 1998;95:6965–6970.^Jones ME, Thorburn AW, Britt KL, Hewitt KN, Wreford NG, Proietto J, Oz OK, Leury BJ, Robertson KM, Yao S, Simpson ER. Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity. Proc Natl Acad Sci U S A. 2000;97:12735–12740.^abBrown LM, Clegg DJ. Central effects of estradiol in the regulation of food intake, body weight, and adiposity. J Steroid Biochem Mol Biol. 2010;122:65–73. ^Mauvais-Jarvis F, Clegg DJ, Hevener AL. The role of estrogens in control of energy balance and glucose homeostasis. Endocr Rev. 2013;34:309–338.^Abdelgadir SE, Resko JA, Ojeda SR, Lephart ED, McPhaul MJ, Roselli CE. Androgens regulate aromatase cytochrome P450 messenger ribonucleic acid in rat brain. Endocrinology. 1994;135:395–401.^Roselli CE, Liu M, Hurn PD. Brain aromatization: classic roles and new perspectives. Semin Reprod Med. 2009;27:207–217.^Merchenthaler I, Lane MV, Numan S, Dellovade TL. Distribution of estrogen receptor alpha and beta in the mouse central nervous system: in vivo autoradiographic and immunocytochemical analyses.^Simerly RB, Chang C, Muramatsu M, Swanson LW. Distribution of androgen and estrogen receptor mRNA-containing cells in the rat brain: an in situ hybridization study.^Gillies GE, McArthur S. Estrogen actions in the brain and the basis for differential action in men and women: a case for sex-specific medicines. Pharmacol Rev. 2010;62:155–198. ^Cederroth CR, Vinciguerra M, Kühne F, Madani R, Doerge DR, Visser TJ, Foti M, Rohner-Jeanrenaud F, Vassalli JD, Nef S. A phytoestrogen-rich diet increases energy expenditure and decreases adiposity in mice. Environ Health Perspect. 2007;115:1467–1473.^Ogawa S, Chan J, Gustafsson JA, Korach KS, Pfaff DW. Estrogen increases locomotor activity in mice through estrogen receptor alpha: specificity for the type of activity. Endocrinology. 2003;144:230–239. ^Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA. Pancreatic extracts in the treatment of diabetes mellitus. Can Med Assoc J. 1922;12:141–146. ^Karamitsos D.T. 2011. The story of insulin discovery. Diabetes Res. Clin. Pract. 93(Suppl 1):S2–S8. 10.1016/S0168-8227(11)70007-9 ^Gavin JR, et al. Insulin-dependent regulation of insulin receptor concentrations: a direct demonstration in cell culture. Proc Natl Acad Sci USA. 1974;71:84–88. ^Freychet P, Roth J, Neville DM., Jr Insulin receptors in the liver: specific binding of (125 I)insulin to the plasma membrane and its relation to insulin bioactivity. Proc Natl Acad Sci USA. 1971;68:1833–1837. ^Kasuga M, Zick Y, Blithe DL, Crettaz M, Kahn CR. Insulin stimulates tyrosine phosphorylation of the insulin receptor in a cell-free system. Nature. 1982;298:667–669. ^ Ebina Y, et al. The human insulin receptor cDNA: the structural basis for hormone-activated transmembrane signalling. Cell. 1985;40:747–758. ^Ullrich A, et al. Human insulin receptor and its relationship to the tyrosine kinase family of oncogenes. Nature. 1985;313:756–761.^Ullrich A, et al. Human insulin receptor and its relationship to the tyrosine kinase family of oncogenes. Nature. 1985;313:756–761.^Hubbard, S. R. (2013). The insulin receptor: both a prototypical and atypical receptor tyrosine kinase. Cold Spring Harbor Perspectives in Biology, 5, a008946^Anthony JC, Reiter AK, Anthony TG, Crozier SJ, Lang CH, MacLean DA, Kimball SR, and Jefferson LS. Orally administered leucine enhances protein synthesis in skeletal muscle of diabetic rats in the^Sinaud S, Balage M, Bayle G, Dardevet D, Vary TC, Kimball SR, Jefferson LS, and Grizard J. Diazoxide-induced insulin deficiency greatly reduced muscle protein synthesis in rats: involvement of eIF4E. Am J Physiol Endocrinol Metab 276:E50–E61, 1999.^Preedy VR and Garlick PJ. The response of muscle proteinsynthesis to nutrient intake in postabsorptive rats: the role ofinsulin and amino acids. Biosci Rep 6: 177–183, 1986.^Pham PT, Heydrick SJ, Fox HL, Kimball SR, Jefferson LS, and Lynch CJ. Assessment of cell signaling pathways in the regulation of mTOR by amino acids in rat adipocytes. J Cell Biochem 79: 427–441, 2000.^Campbell LE, Wang X, and Proud CG. Nutrients differentially regulate multiple translation factors and their control by insulin. Biochem J 344: 433–441, 1999.^Anton J. M. Wagenmakers,corresponding author 1 ,* Juliette A. Strauss, 1 Sam O. Shepherd, 1 Michelle A. Keske, 2 and Matthew Cocks.Increased muscle blood supply and transendothelial nutrient and insulin transport induced by food intake and exercise: effect of obesity and ageing.2016 Apr 15; 594(8): 2207–2222.^Clerk LH, Vincent MA, Jahn LA, Liu Z, Lindner JR, Barrett EJ. Obesity blunts insulinmediated microvascular recruitment in human forearm muscle. Diabetes. 2006;55(5):1436-1442^Clerk LH, Vincent MA, Barrett EJ, Lankford MF, Lindner JR. Skeletal muscle capillary responses to insulin are abnormal in late-stage diabetes and are restored by angiotensinconverting enzyme inhibition. American journal of physiology Endocrinology and metabolism. 2007;293(6):E1804-1809.^Vincent MA, Clerk LH, Lindner JR, et al. Mixed meal and light exercise each recruit muscle capillaries in healthy humans. American journal of physiology Endocrinology and metabolism. 2006;290(6):E1191-1197.^Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the international Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16):1640–1645.^Guallar-Castillon P, Perez RF, Lopez Garcia E, et al. Magnitude and management of metabolic syndrome in Spain in 2008–2010: the ENRICA study. Rev Esp Cardiol. 2014;67(5):367–373.^Prasad DS, Kabir Z, Dash AK, et al. Prevalence and risk factors for metabolic syndrome in Asian Indians: a community study from urban eastern India. J Cardiovasc Dis Res. 2012;3(3):204–211.^Ford ES, Li C, Zhao G, et al. Prevalence of the metabolic syndrome among U.S. adolescents using the definition from the International Diabetes Federation. Diabetes Care. 2008;31(3):587–589.^abKoopman R, Zorenc AHG, Gransier RJJ, Cameron-Smith D, and van Loon LJC. Increase in S6K1 phosphorylation in human skeletal muscle following resistance exercise occurs mainly in type II muscle fibers. Am J Physiol Endocrinol Metab 290: E1245–52, 2006.^M.-Y. Chien, L.-Y. Wang, H.-C. Chen, The relationship of sleep duration with obesity and sarcopenia in community-dwelling older adults. Gerontology 61, 399–406 (2015).^M. Monico-Neto, S. Q. Giampá, K. S. Lee, C. M. de Melo, H. de Sá Souza, M. Dáttilo, P. A. Minali, P. H. Santos Prado, S. Tufik, M. T. de Mello, H. K. M. Antunes, Negative energy balance induced by paradoxical sleep deprivation causes multicompartmental changes in adipose tissue and skeletal muscle. Int. J. Endocrinol. 2015, 908159 (2015).^Jefferson LS, Rannels DE, Munger BL, and Morgan HE. Insulin in the regulation of protein turnover in heart and skeletal muscle. Fed Proc 33: 1098–1104, 1974.^Karinch AM, Kimball SR, Vary TC, and Jefferson LS. Regulation of eukaryotic initiation factor-2B activity in muscle of diabetic rats. Am J Physiol Endocrinol Metab 264: E101–E108, 1993.^Kimball SR, Vary TC, and Jefferson LS. Regulation of protein synthesis by insulin. Annu Rev Physiol 56: 321–348, 1994.^Anthony JC, Reiter AK, Anthony TG, Crozier SJ, Lang CH, MacLean DA, Kimball SR, and Jefferson LS. Orally administered leucine enhances protein synthesis in skeletal muscle of diabetic rats in the absence of increases in 4E-BP1 or S6K1 phosphorylation. Diabetes 51: 928–936, 2002.^Park YW, Zhu S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield SB. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988–1994. Arch Intern Med. 2003;163:427–436.^ Yki-Jarvinen H. Sex and insulin sensitivity. Metabolism. 1984;33:1011–1015. ^Hevener AL, Olefsky JM, Reichart D, et al. Macrophage PPAR γ is required for normal skeletal muscle and hepatic insulin sensitivity and full antidiabetic effects of thiazolidinediones. J Clin Invest. 2007;117:1658–1669. ^Choi CS, Fillmore JJ, Kim JK, et al. Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance. J Clin Invest. 2007;117:1995–2003. ^Frias JP, Macaraeg GB, Ofrecio J, Yu JG, Olefsky JM, Kruszynska YT. Decreased susceptibility to fatty acid-induced peripheral tissue insulin resistance in women. Diabetes. 2001;50:1344–1350.^Hevener A, Reichart D, Janez A, Olefsky J. Female rats do not exhibit free fatty acid-induced insulin resistance. Diabetes. 2002;51:1907–1912. ^ Djouadi F, Weinheimer CJ, Saffitz JE, et al. A gender-related defect in lipid metabolism and glucose homeostasis in peroxisome proliferator-activated receptor α-deficient mice. J Clin Invest. 1998;102:1083–1091. ^Hong J, Stubbins RE, Smith RR, Harvey AE, Nunez NP. Differential susceptibility to obesity between male, female and ovariectomized female mice. Nutr J. 2009;8:11.^ Rincon J, Holmang A, Wahlstrom E O, Lonnroth P, Bjorntorp P, Zierath J R, Wallberg-Henriksson H. Diabetes. 1996;45:615–621. ^Hope P J, Turnbull H, Breed W, Morley J E, Horowitz M, Wittert G A. Physiol Behav. 2000;69:463–470. ^Rogers NH, Witczak CA, Hirshman MF, Goodyear LJ, Greenberg AS. Estradiol stimulates Akt, AMP-activated protein kinase (AMPK) and TBC1D1/4, but not glucose uptake in rat soleus. Biochem Biophys Res Commun. 2009;382:646–650. ^Gorres BK, Bomhoff GL, Morris JK, Geiger PC. In vivo stimulation of oestrogen receptor α increases insulin-stimulated skeletal muscle glucose uptake. J Physiol. 2011;589:2041–2054. ^Bryzgalova G, Gao H, Ahren B, et al. Evidence that oestrogen receptor-α plays an important role in the regulation of glucose homeostasis in mice: insulin sensitivity in the liver. Diabetologia. 2006;49:588–597.^Wiik A, Gustafsson T, Esbjornsson M, et al. Expression of oestrogen receptor α and β is higher in skeletal muscle of highly endurance-trained than of moderately active men. Acta Physiol Scand. 2005;184:105–112. ^Fu MH, Maher AC, Hamadeh MJ, Ye C, Tarnopolsky MA. Exercise, sex, menstrual cycle phase, and 17β-estradiol influence metabolism-related genes in human skeletal muscle. Physiol Genomics. 2009;40:34–47. ^Rogers NH, Witczak CA, Hirshman MF, Goodyear LJ, Greenberg AS. Estradiol stimulates Akt, AMP-activated protein kinase (AMPK) and TBC1D1/4, but not glucose uptake in rat soleus. Biochem Biophys Res Commun. 2009;382:646–650.^Riant E, Waget A, Cogo H, Arnal JF, Burcelin R, Gourdy P. Estrogens protect against high-fat diet-induced insulin resistance and glucose intolerance in mice. Endocrinology. 2009;150:2109–2117.^Ordonez P, Moreno M, Alonso A, Llaneza P, Diaz F, Gonzalez C. 17β-Estradiol and/or progesterone protect from insulin resistance in STZ-induced diabetic rats. J Steroid Biochem Mol Biol. 2008;111:287–294. ^Stitt TN, Drujan D, Clarke BA, et al. The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. Mol Cell. 2004;14:395–403. ^Pfeilschifter J, Koditz R, Pfohl M, Schatz H. Changes in proinflammatory cytokine activity after menopause. Endocr Rev. 2002;23:90–119. ^Sites CK, Toth MJ, Cushman M, et al. Menopause-related differences in inflammation markers and their relationship to body fat distribution and insulin-stimulated glucose disposal. Fertil Steril. 2002;77:128–135.