減肥的時候是先減皮下脂肪還是內臟上的脂肪呢？

一、人體脂肪的消耗有明確的位置優先級：優先消耗內臟脂肪與許多自媒體說的不太一樣，人體的脂肪消耗并不是全身均勻的。雖然有少數研究得出減肥時消耗的內臟脂肪比皮下脂肪少[1][2]，但大多數研究指出『減肥過程中內臟脂肪比皮下脂肪消耗更多』。

Kelley等人2004年在權威期刊《Diabetes Care》上發表了一篇論文，針對39名肥胖的2型糖尿病患者（平均體重100kg，平均BMI35）進行減肥實驗（節食+藥物），26周受試者們減去的內臟脂肪（26%）明顯高于皮下脂肪（15%）[3]。

原文截圖

查了下《Diabetes Care》的因子高達18.1，1區的，比較可信。

查詢頁面

Ross等人2004年招募了54名肥胖婦女（平均腰圍110CM，平均BMI32），其中15人采用節食減肥，17人運動減肥[4]。結果節食減肥組減去的內臟脂肪（20.8%）比腹部皮下脂肪（8.9%）更多；運動組減的內臟脂肪（30%）也比皮下脂肪多（16.9%）。

Subcuttaneous fat是皮下脂肪，visceral fat是內臟脂肪

除了這兩個，還有大量關于節食的研究，都支持上述結論：

Weinser等人2001年：23名肥胖女性，26周減去內臟脂肪40.7%、皮下脂肪%33.1[5]；Gower等人2002年：19名肥胖女性，26周減去內臟脂肪38.5%、皮下脂肪30.3%[6]；Pascuali等人2000年：10名肥胖女性，4周減去內臟脂肪8.3%、皮下脂肪6.5%[7]；Alvarez等人2005年：6名肥胖男性，13周減去內臟脂肪23.9%、皮下脂肪%17.7[8]；Rice等人1999年：9名肥胖男性，16周減去內臟脂肪35%、皮下脂肪25%[9]；Weits等人1989年：20名肥胖女性，12周減去內臟脂肪15.1%、皮下脂肪10.6%[10]；Okura等人2002年：14名肥胖女性，14周減去內臟脂肪40%、皮下脂肪28%[11]；Fujioka等人1991年：26名肥胖女性，8周減去內臟脂肪33.3%、皮下脂肪22.6%[12]；Janssen等人1999年：13名肥胖女性，16周減去內臟脂肪28.6%、皮下脂肪18.8%[13]；Tchernof等人2002年：25名肥胖女性，14周減去內臟脂肪36.4%、皮下脂肪23.7%[14]；Thong等人2000年：14名肥胖男性，12周減去內臟脂肪25.2%、皮下脂肪15.7%[15]；Tiikainen等人2003年：11名肥胖女性，17周減去內臟脂肪23%、皮下脂肪13%[16]；Tiikainen等人同年的另一項研究中12名肥胖女性，17周減去內臟脂肪29%、皮下脂肪14%[16]；ROSE等人2000年：14名肥胖男性，13周減去內臟脂肪28.1%、皮下脂肪15.6%[17]；Gambinery等人2003年：7名肥胖女性，26周減去內臟脂肪18.8%、皮下脂肪8.4%[18]；采用節食加運動的研究，結論也類似：

Park等人2004年：47名肥胖者，12周減去內臟脂肪23.8%、皮下脂肪19.9%[19]；Nakamura等人2000年：60名肥胖女性，13周減去內臟脂肪12.5%、皮下脂肪8.9%[20]；Park等人2005年：36名肥胖女性，12周減去內臟脂肪22.5%、皮下脂肪14.8%[21]；Okura等人2005年：71名肥胖女性，14周減去內臟脂肪39%、皮下脂肪24%[22]；Pare等人2001年：45名肥胖男性，52周減去內臟脂肪19.9%、皮下脂肪10.1%[23]；采用節食加減肥藥物的研究，依然支持上述結論：

Kelley等人2004年（奧利司他）：19名肥胖者，26周減去內臟脂肪28%、皮下脂肪16%[24]；Tiikk等人2004年（奧利司他）：24名肥胖女性，21周減去內臟脂肪27%、皮下脂肪14%[25]；Kim等人2004年（鹽酸西布曲明）：28名肥胖女性，12周減去內臟脂肪19.9%、皮下脂肪16.5%[26]；Kamel等人2000年：17名肥胖男性（鹽酸西布曲明），26周減去內臟脂肪37.5%、皮下脂肪24%[27]；19名肥胖女性，26周減去內臟脂肪43.3%、皮下脂肪20.1[27]；Yip等人2001年：20名肥胖女性（鹽酸西布曲明），24周減去內臟脂肪%35.5、皮下脂肪%26.2[28]；總之，不管是節食、運動、藥物等一切減肥方式（還有胃部手術的沒放上來），『減肥過程中內臟脂肪一般比皮下脂肪消耗更多』，所以人體消耗脂肪，是有部位的優先級的。

二、同樣是人身上的肥肉，『脂肪』和『脂肪』是不同的按顏色，人體脂肪可以分白色脂肪和棕色脂肪[29][30]，以及可以演化成棕色脂肪的米色脂肪[31]；按部位，脂肪有皮下、內臟、骨骼肌內脂、心肌脂等。

脂肪組織不僅是脂肪滴的容器，也是調節內分泌的器官。脂肪細胞中富含神經、血管和各種結締組織[32]，能分泌多種細胞因子，調節食欲、能量代謝、免疫功能和生殖[33]；

皮下脂肪和內臟脂肪都是白色脂肪組織，但它們具有不同的作用（如內分泌）。皮下脂肪分泌瘦素，對健康可能更有益或者至少無害[34]，而內臟脂肪分泌各種促炎物質，如白介素IL-6、C-反應蛋白CRP[33]等，它們與代謝綜合征有關[35][36][37][38][39][40]。

說個題外話，皮下脂肪和內臟脂肪的代謝特性差異，也造成了絕經前女性的代謝疾病率明顯低于男性[41][42][43][44][45][46][47]；并且即便男性和女性的身體脂肪總量相等這種疾病率差異依然存在[48][49]。這主要因為雌激素把脂肪從『內臟』向『腿皮下』“轉移”[50][51][52][53][54][55]，如果全身脂肪總量相同，男性的內臟脂肪量可能是女性的2倍[56]。

雌激素與脂肪分布

內臟和皮下脂肪脂肪的代謝特性也有不同。Virtanen等人通過同位素標記的葡萄糖，證明了內臟脂肪對葡萄糖的攝取明顯高于皮下脂肪[57]；Andersson等人讓受試者口服了帶有同位素標記的甘油三酯，發現內臟脂肪（腹腔網膜）對甘油三酯的攝取顯著高于皮下脂肪50%以上[58]。

三、相對而言，內臟脂肪更容易被釋放、被身體利用這不是什么新鮮觀點，早就是主流結論了。最典型的是Robert等人2007年發表在權威期刊《Diabetes》上的研究，用碳14同位素標記方法追蹤來自內臟和非內臟脂肪酸[59]。

封面

這篇論文包含了AB兩個研究。

A研究中，內臟脂肪酸釋放為60±7%，非內臟脂肪酸釋放24±6%；B研究中內臟脂肪酸釋放為54±3%，非內臟脂肪酸釋放16±5%。這些數據很好的說明了內臟脂肪具有更強的代謝活躍性，更容易被攝取和利用。

內臟脂肪酸釋放（白）VS非內臟脂肪酸釋放（黑）

1991年，Jensen等人也用上述方法觀察研究了20名女性（8人上身肥胖/6人下身體肥胖/6人不肥胖）餐后脂肪酸的總釋放情況[60]：

上身肥胖者的脂肪酸釋放為161±16微摩/分鐘；下身肥胖者的脂肪酸釋放為為為111+/-9微摩/分鐘；非肥胖者的脂肪酸釋放為為92+/-9微摩/分鐘。同位素標記追蹤的結果證明了腿部脂肪釋放的脂肪酸明顯少于內臟脂肪。Guo等人也用類似方法，研究了8名上身肥胖和下身肥胖的女性餐后脂肪酸的代謝，發現了內臟脂肪和下半身堆積的脂肪，在餐后脂肪酸流量方面有顯著差異[61]。

上身肥胖組的女性內臟脂肪酸釋放流為275±45微摩爾/分鐘；下半身肥胖組的女性內臟脂肪酸釋放流為88±24微摩爾/分鐘。這些數據證明了內臟脂肪的代謝流動性明顯高于皮下脂肪，優先被釋放，優先被消耗。

類似的研究不少[62][63][64][65]，結論從性質上相似，就不挨個細說了。總之，內臟脂肪酸的代謝活躍性相對于其他部位更強、更容易被釋放出來利用。

這也解釋了為什么，很多女生發現減肥初期肚子減得最明顯，胸和屁股減得少一些，減肥之后形體得到了美化，腰臀比降低了。

四、內臟脂肪對脂解激素的敏感性更高脂解激素，指的是人體處于禁食、運動或能量不足的狀態時器官分泌一些激素。

這些激素從器官（腎臟、胰腺等）被釋放，隨血液運輸到脂肪細胞，與其表面的受體結合，然后引發一系列反應，讓脂肪細胞中的脂肪酸被釋放出來，供各器官和大腦使用。

典型的脂解激素有胰高血糖素[66]、腎上腺素[67]和去甲腎上腺素[68]等；其中，腎上腺素被認為是最主要的一種。

脂解激素

內臟脂肪對脂解激素更敏感，跟受體有很大關系。

Jeong等人研究了女性皮下（大腿/腹部）和內臟（腹腔網膜）脂肪，發現內臟脂肪細胞與皮下脂肪細胞表面的脂解激素（如腎上腺素）的受體位點數量、分布都有差異[69]：皮下脂肪細胞上的脂解激素（腎上腺素）受體β數量比α-2要少，而內臟脂肪細胞上的β受體跟α-2一樣多。

1990年，Arner等人研究了32名非肥胖男女腹部和臀部脂肪細胞中β腎上腺素受體，發現腹部脂肪細胞上的β腎上腺素受體數量幾乎是臀部脂肪細胞上的2倍，而且腹部脂肪細胞上的腎上腺素受體β1、β2、β3[70]十分活躍。這可在很大程度上解釋內臟脂肪細胞對脂解激素的敏感反應和優先燃燒。

當然，既然有脂解，也就有抗脂解。顧名思義，抗脂解就是對抗脂肪分解，“把脂肪酸關在脂肪細胞里不讓它跑出來被燃燒”。

Arner等人還報道說，抗脂解激素（如胰島素）的受體，在皮下脂肪更活躍[70]，但在內臟脂肪細胞中不活躍[71][72]。因此抗脂解激素很難把內臟脂肪制約在脂肪細胞中，結果內臟脂肪容易不受管控的逸出，在供能上優先級較高。

作為一個典型證據，Meek等人對26人注射胰島素后，腿部皮下脂肪組織的脂肪酸釋放幾乎完全被制止，而內臟脂肪依然在釋放脂肪酸（雖然減少了65%）[73]。

打個有趣的彼方，就像現在疫情來了要封閉清零：

脂肪酸像是居民，腿臀部和內臟就是不同的小區；脂解激素有點像快遞員，他們要讓小區居民出來拿快遞；抗脂解激素就是負責封閉小區的居委會，不讓小區居民出來；腿臀部小區居民比較聽居委會的話，對外賣的誘惑視若無睹，老老實實待在家里；內臟小區居民不太聽居委會話，對快遞員很熱情，總是跑到外面去拿快遞。

五、內臟脂肪的供能優先級：地理位置優勢

我們已經知道，在禁食/饑餓/運動/能量不足期間，腎臟/胰腺等器官分泌脂解激素作用于脂肪細胞，釋放脂肪酸出來供身體使用。

但是釋放的脂肪酸，并不是直接到了各種器官，而是先去肝臟。Michele等人報告[74]在禁食/能量不足狀態下，脂肪細胞釋放的脂肪酸（至少大部分）先到肝臟，再到肌肉和其他組織。脂肪細胞為什么會開始釋放脂肪酸？我們剛剛解釋過，脂解激素刺激。

把兩張圖拼起來就是這樣：

粗略框架

這樣，整個流程就大體上完整了。所以我們應該清楚，脂肪組織釋放的脂肪酸，并不是直接去了肌肉/其他器官，而是先去了肝臟，在肝臟合成TG（甘油三酯），然后再送往肌肉/其他器官。

因為肝臟是能量代謝的中心[74][75]。

這和我們的主題（內臟脂肪供能的優先級）有什么關系？答案是，相比大腿而言，內臟脂肪離肝臟近，向肝臟供能便捷——門靜脈[76][77][78]。

門靜脈

雖然這種說法聽起來有點像地攤文學，但確實在許多科學文獻都有提及：『門靜脈理論』[79][80]。即：因為網膜、腸系膜等內臟脂肪組織的血管直接連入門靜脈，可以將大量的脂肪酸釋放到門靜脈中，門靜脈的脂肪酸濃度可顯著高于動脈脂肪酸濃度，使肝臟沐浴在高濃度的脂肪酸流中[81][82]。

Soren等人早在2004年就證明[83]：男性和女性受試者的內臟脂肪越多（越胖），肝臟得到的脂肪酸中，來自內臟脂肪的比例就越高。

男性和女性受試者從內臟脂肪組織脂解產生脂肪酸，向肝臟輸送的百分比

Soren等人的研究是一個強有力的證據，證明了餐后內臟肥胖的人的肝臟暴露于更高濃度的游離脂肪酸。這也解釋了為什么內臟脂肪在供能上，相對于大腿/皮下脂肪，具有更高的優先級。

總之，減肥一定是先減內臟脂肪、或者說內臟脂肪動用比例較大的。

References1. ^Okura T, Nakata Y, Tanaka K. Effects of exercise intensity on physical fitness and risk factors for coronary heart disease. Obes Res 2003; 11: 1131–1139.

2. ^ Weinsier RL, Hunter GR, Gower BA, Schutz Y, Darnell BE, Zuckerman PA. Body fat distribution in white and black women: different patterns of intraabdominal and subcutaneous abdominal adipose tissue utilization with weight loss. Am J Clin Nutr 2001; 74: 631–636.

3. ^Kelley DE, Kuller LH, McKolanis TM, Harper P, Mancino J, Kalhan S. Effects of moderate weight loss and orlistat on insulin resistance, regional adiposity, and fatty acids in type 2 diabetes. Diabetes Care 2004; 27: 33–40.

4. ^Ross R, Janssen I, Dawson J, Kungl AM, Kuk JL, Wong SL et al. Exercise-induced reduction in obesity and insulin resistance in women: a randomized controlled trial. Obes Res 2004; 12: 789–798.

5. ^Weinsier RL, Hunter GR, Gower BA, Schutz Y, Darnell BE, Zuckerman PA. Body fat distribution in white and black women: different patterns of intraabdominal and subcutaneous abdominal adipose tissue utilization with weight loss. Am J Clin Nutr 2001; 74: 631–636.

6. ^ Gower BA, Weinsier RL, Jordan JM, Hunter GR, Desmond R. Effects of weight loss on changes in insulin sensitivity and lipid concentrations in premenopausal African American and White women. Am J Clin Nutr 2002; 76: 923–927.

7. ^ Pasquali R, Gambineri A, Biscotti D, Vicennati V, Gagliardi L, Colitta D et al. Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome. J Clin Endocrinol Metab 2000; 85: 2767–2774.

8. ^Alvarez GE, Davy BM, Ballard TP, Beske SD, Davy KP. Weight loss increases cardiovagal baroreflex function in obese young and older men. Am J Physiol Endocrinol Metab 2005; 289: E665–E669.

9. ^Rice B, Janssen I, Hudson R, Ross R. Effects of aerobic or resistance exercise and/or diet on glucose tolerance and plasma insulin levels in obese men. Diabetes Care 1999; 22: 684–691.

10. ^Weits T, van der Beek EJ, Wedel M, Hubben MW, Koppeschaar HP. Fat patterning during weight reduction: a multimode investigation. Neth J Med 1989; 35: 174–184.

11. ^Okura T, Tanaka K, Nakanishi T, Lee DJ, Nakata Y, Wee SW et al. Effects of obesity phenotype on coronary heart disease risk factors in response to weight loss. Obes Res 2002; 10: 757–766

12. ^Fujioka S, Matsuzawa Y, Tokunaga K, Kawamoto T, Kobatake T, Keno Y et al. Improvement of glucose and lipid metabolism associated with selective reduction of intra-abdominal visceral fat in premenopausal women with visceral fat obesity. Int J Obes 1991; 15: 853–859.

13. ^Janssen I, Ross R. Effects of sex on the change in visceral, subcutaneous adipose tissue and skeletal muscle in response to weight loss. Int J Obes Relat Metab Disord 1999; 23: 1035–1046.

14. ^Tchernof A, Nolan A, Sites CK, Ades PA, Poehlman ET. Weight loss reduces C-reactive protein levels in obese postmenopausal women. Circulation 2002; 105: 564–569.

15. ^Thong FS, Hudson R, Ross R, Janssen I, Graham TE. Plasma leptin in moderately obese men: independent effects of weight loss and aerobic exercise. Am J Physiol Endocrinol Metab 2000; 279: E307–E313.

16. ^abTiikkainen M, Bergholm R, Vehkavaara S, Rissanen A, Hakkinen AM, Tamminen M et al. Effects of identical weight loss on body composition and features of insulin resistance in obese women with high and low liver fat content. Diabetes 2003; 52: 701–707.

17. ^Ross R, Dagnone D, Jones PJ, Smith H, Paddags A, Hudson R et al. Reduction in obesity and related comorbid conditions after dietinduced weight loss or exercise-induced weight loss in men. A randomized, controlled trial. Ann Intern Med 2000; 133: 92–103.

18. ^Gambineri A, Pagotto U, Tschop M, Vicennati V, Manicardi E, Carcello A et al. Anti-androgen treatment increases circulating ghrelin levels in obese women with polycystic ovary syndrome. J Endocrinol Invest 2003; 26: 629–634.

19. ^Park HS, Sim SJ, Park JY. Effect of weight reduction on metabolic syndrome in Korean obese patients. J Korean Med Sci 2004; 19: 202–208.

20. ^Nakamura M, Tanaka M, Kinukawa N, Abe S, Itoh K, Imai K et al. Association between basal serum and leptin levels and changes in abdominal fat distribution during weight loss. J Atheroscler Thromb 2000; 6: 28–32.

21. ^ Park HS, Lee K. Greater beneficial effects of visceral fat reduction compared with subcutaneous fat reduction on parameters of the metabolic syndrome: a study of weight reduction programmes in subjects with visceral and subcutaneous obesity. Diabet Med 2005; 22: 266–272.

22. ^Okura T, Nakata Y, Lee DJ, Ohkawara K, Tanaka K. Effects of aerobic exercise and obesity phenotype on abdominal fat reduction in response to weight loss. Int J Obes (London) 2005; 29: 1259–1266.

23. ^Pare A, Dumont M, Lemieux I, Brochu M, Almeras N, Lemieux S et al. Is the relationship between adipose tissue and waist girth altered by weight loss in obese men? Obes Res 2001; 9: 526–534.

24. ^Kelley DE, Kuller LH, McKolanis TM, Harper P, Mancino J, Kalhan S. Effects of moderate weight loss and orlistat on insulin resistance, regional adiposity, and fatty acids in type 2 diabetes. Diabetes Care 2004; 27: 33–40.

25. ^ Tiikkainen M, Bergholm R, Rissanen A, Aro A, Salminen I, Tamminen M et al. Effects of equal weight loss with orlistat and placebo on body fat and serum fatty acid composition and insulin resistance in obese women. Am J Clin Nutr 2004; 79: 22–30.

26. ^Kim DM, Yoon SJ, Ahn CW, Cha BS, Lim SK, Kim KR et al. Sibutramine improves fat distribution and insulin resistance, and increases serum adiponectin levels in Korean obese nondiabetic premenopausal women. Diabetes Res Clin Pract 2004; 66 (Suppl 1): S139–S144.

27. ^abKamel EG, McNeill G, Van Wijk MC. Change in intra-abdominal adipose tissue volume during weight loss in obese men and women: correlation between magnetic resonance imaging and anthropometric measurements. Int J Obes Relat Metab Disord 2000; 24: 607–613.

28. ^Yip I, Go VL, Hershman JM, Wang HJ, Elashoff R, DeShields S et al. Insulin–leptin–visceral fat relation during weight loss. Pancreas 2001; 23: 197–203.

29. ^nnon B, Nedergaard J. Brown adipose tissue: function and physiological significance. Physiological reviews. 2004;84:277–359.

30. ^Enerb?ck S, Jacobsson A, Simpson EM, Guerra C, Yamashita H, Harper ME, Kozak LP. Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese. Nature. 1997;387:90–94.

31. ^Walden TB, Hansen IR, Timmons JA, Cannon B, Nedergaard J. Recruited vs. nonrecruited molecular signatures of brown, "brite," and white adipose tissues. American journal of physiology Endocrinology and metabolism. 2012;302:E19–31.

32. ^Bartness TJ, Vaughan CH, Song CK. Sympathetic and sensory innervation of brown adipose tissue. Int J Obes (Lond) 2010b;34(Suppl 1):S36–42.

33. ^abTrujillo ME, Scherer PE. Adipose tissue-derived factors: impact on health and disease. Endocr.Rev. 2006;27:762–778.

34. ^Lee MJ, Wu Y, Fried SK. Adipose tissue heterogeneity: mplication of depot differences in adipose tissue for obesity complications. Molecular aspects of medicine. 2013;34:1–11.

35. ^ Bjorntorp P. Metabolic implications of body fat distribution.Diabetes Care 1991; 14: 1132±1143.

36. ^Kissebah AH, Videlingum N, Murray R, et al. Relation of body fat distribution to metabolic complications of obesity. J Clin Endocrinol Metab 1982;54:254-60.

37. ^Abate N, Garg A, Peshock RM, StrayGundersen J, Grundy SM. Relationships of generalized and regional adiposity to insulin sensitivity in men. J Clin Invest 1995;96: 88-98.

38. ^Planas A, Clará A, Pou JM, et al. Relationship of obesity distribution and peripheral arterial occlusive disease in elderly men. Int J Obesity 2001;25:1068–70

39. ^Kete I, Mariken, Volman M, et al. Superiority of skinfold measurements and waist over waist-to-hip ratio for determination of body fat distribution in a population-based cohort of Caucasian Dutch adults. Eur J Endocrinol 2007;156:655–61.

40. ^Alexander JK. Obesity and coronary heart disease. Am J Med Sci 2001;321:215–24.

41. ^Lemer D J, Kannel WB (1986) Patterns of coronary heart diseases morbidity and mortality in the sexes: a 26-year followup of the Framingham population. Am Heart J 11:383-390

42. ^Wingard DL, Suarez L, Barrett-Connor E (1983) The sex differential in mortality from all causes and ischemic heart disease. Am J Epidemio1117:165-172

43. ^Freedman DS, Jacobsen S J, Barboriak JJ et al. (1990) Body fat distribution and male/female differences in lipids and lipoproteins. Circulation 81:1498-1506

44. ^Larsson B, Bengtsson C, Bj6rntorp Pet al. (1992) Is abdominal body fat distribution a major explanation for the sex difference in the incidence of myocardial infarction? Am J Epidemio1135: 266-273

45. ^Seidell JC, Cigolini M, Charzewska Jet al. (1991) Fat distribution and gender differences in serum lipids in men and women from four European communities. Atherosclerosis 87:203-210

46. ^Despr6s JR Moorjani S, Fefland Met al. (1989) Adipose tissue distribution and plasma lipoprotein levels in obese women: importance of intra-abdominal fat. Arteriosclerosis 9:203-210

47. ^Despr6s JP, Moorjani S, Lupien PJ, Tremblay A, Nadeau A, Bouchard C (1990) Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. Arteriosclerosis 10: 497-511

48. ^ Despr6s JP, Allard C, Tremblay A, Talbot J, Bouchard C (1985) Evidence for a regional component of body fatness in the association with serum lipids in men and women. Metabolism 34:967-973

49. ^Krotkiewski M, Bj6rntorp P, Sj6strOm L, Smith U (1983) Impact of obesity on metabolism in men and women. Importance of regional adipose tissue distribution. J Clin Invest 72: 1150-1162

50. ^Wajchenberg BL. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev 2000;21:697–738.

51. ^Krotkiewski M, Bjorntorp P, Sjostrom L, Smith U. Impact of obesity on metabolism in men and women. Importance of regional adipose tissue distribution. J Clin Invest 1983;72:1150–62.

52. ^Mayes JS, Watson GH. Direct effects of sex steroid hormones on adipose tissues and obesity. Obes Rev 2004;5:197–216.

53. ^Lemer D J, Kannel WB (1986) Patterns of coronary heart diseases morbidity and mortality in the sexes: a 26-year followup of the Framingham population. Am Heart J 11:383-390

54. ^Kvist H, Chowdury B, Gang~rd U, Tyl6n U, Sj6str0m L (1988) Total and visceral adipose-tissue volumes derived from measurements with computed tomography in adult men and women: predictive equations. Am J Clin Nutr 48:1351-1361

55. ^SjOstr6m L, Kvist H (1988) Regional body fat measurements with computed tomography-scan and evaluation of anthropometric predictions. Acta Med Scand [Suppl] 723:169-177

56. ^Lemieux S, Prud'homme D, Bouchard C, Tremblay A, Despr6s JP (1993) Sex differences in the relation of visceral adipose tissue to total body fatness. Am J Clin Nutr 58:463-467

57. ^Virtanen KA, L?nnroth P, Parkkola R, Peltoniemi P, Asola M, Viljanen T, et al. Glucose uptake and perfusion in subcutaneous and visceral adipose tissue during insulin stimulation in nonobese and obese humans. J Clin Endocrinol Metab. 2002

58. ^M?rin P, Andersson B, Ottosson M, Olbe L, Chowdhury B, Kvist H, et al. The morphology and metabolism of intraabdominal adipose tissue in men. Metabolism. 1992

59. ^Nelson RH, Basu R, Johnson CM, Rizza RA, Miles JM. Splanchnic spillover of extracellular lipase-generated fatty acids in overweight and obese humans. Diabetes. 2007;56:2878–2884.

60. ^Martin ML, Jensen MD. Effects of body fat distribution on regional lipolysis in obesity. J. Clin. Invest. 1991;88:609–613.

61. ^Guo ZK, Hensrud DD, Johnson CM, Jensen MD. Regional postprandial fatty acid metabolism in different obesity phenotypes. Diabetes. 1999;48:1586–1592.

62. ^Jensen MD. Gender differences in regional fatty acid metabolism before and after meal ingestion. J. Clin. Invest. 1995;96:2297–2303.

63. ^Jensen MD, Johnson CM. Contribution of leg and splanchnic free fatty acid (FFA) kinetics to postabsorptive FFA flux in men and women. Metabolism. 1996;45:662–666.

64. ^Basu A, et al. Systemic and regional free fatty acid metabolism in type 2 diabetes. Am. J. Physiol. Endocrinol. Metab. 2001;280:E1000–E1006.

65. ^Meek S, Nair KS, Jensen MD. Insulin regulation of regional free fatty acid metabolism. Diabetes. 1999;48:10–14.

66. ^Birbrair A., Zhang T., Wang Z.M., Messi M.L., Enikolopov G.N., Mintz A., Delbono O. Role of pericytes in skeletal muscle regeneration and fat accumulation. Stem Cells Dev. 2013;22:2298–2314.

67. ^Lafontan M., Langin D. Lipolysis and lipid mobilization in human adipose tissue. Prog. Lipid Res. 2009;48:275–297.

68. ^Jaworski K., Sarkadi-Nagy E., Duncan R.E., Ahmadian M., Sul H.S. Regulation of triglyceride metabolism. IV. Hormonal regulation of lipolysis in adipose tissue. Am. J. Physiol. Gastrointest. Liver Physiol. 2007;293:G1–G4.

69. ^ Mi-Jeong Lee,Susan K. Fried.Depot-Specific Biology of Adipose Tissues: Links to Fat Distribution and Metabolic Risk.Book Editor(s):Todd Leff,James G. Granneman.

70. ^abP Arner 1.Differences in lipolysis between human subcutaneous and omental adipose tissues.Ann Med. 1995 Aug;27(4):435-8.

71. ^Leibel RL, Edens NK, Fried SK. Physiologic basis for the control of body fat distribution in humans. Annu.Rev.Nutr. 1989a;9:417–443.

72. ^Lonnqvist F, Thorne A, Large V, Arner P. Sex differences in visceral fat lipolysis and metabolic complications of obesity. Arterioscler.Thromb.Vasc.Biol. 1997;17:1472–1480.

73. ^Meek SE, Nair KS, Jensen MD. Insulin regulation of regional free fatty acid metabolism. Diabetes. 1999;48:10–14.

74. ^abMichele Alves-Bezerra and David E. Cohen.Triglyceride metabolism in the liver.Compr Physiol. Author manuscript; available in PMC 2019 Feb 15.

75. ^Vasconcellos R, Alvarenga EC, Parreira RC, Lima SS, and Resende RR. Exploring the cell signalling in hepatocyte differentiation. Cell Signal 28: 1773–1788, 2016.

76. ^Antonio Manenti 1, Gianrocco Manco 2, Alberto Farinetti 2, Luca Roncati 3.The intrahepatic branches of portal vein: a relevant surgical topic.Surgery. 2021 May;169(5):1265.

77. ^ Z C Edelson.Preduodenal portal vein.Am J Surg. 1974 May;127(5):599-600.

78. ^Connie Ju? , Xin Li , Sameer Gadani , Baljendra Kapoor , Sasan Partovi.Pfortaderthrombose: Diagnose und endovaskul?res Management.Portal Vein Thrombosis: Diagnosis and Endovascular Management.

79. ^Bjorntorp P. “Portal” adipose tissue as a generator of risk factors for cardiovascular disease and diabetes.

80. ^R N Bergman 1.Non-esterified fatty acids and the liver: why is insulin secreted into the portal vein?.Diabetologia. 2000 Jul;43(7):946-52.

81. ^Michael D. Jensen.Role of Body Fat Distribution and the Metabolic Complications of Obesity.J Clin Endocrinol Metab. 2008 Nov; 93(11 Suppl 1): S57–S63.

82. ^J Svedberg, G Str?mblad, A Wirth, U Smith, and P Bj?rntorp.Fatty acids in the portal vein of the rat regulate hepatic insulin clearance.J Clin Invest. 1991 Dec; 88(6): 2054–2058.

83. ^Soren Nielsen,1 ZengKui Guo,1 C. Michael Johnson,2 Donald D. Hensrud,1 and Michael D. Jensen1.Splanchnic lipolysis in human obesity.J Clin Invest. 2004 Jun 1; 113(11): 1582–1588.

84. ^eters S. J., Dyck D. J., Bonen A., Spriet L. L. Effects of epinephrine on lipid metabolism in resting skeletal muscle. The American Journal of Physiology. 1998;275(2 Part 1):E300–E309.

85. ^Dyck D. J., Bonen A. Muscle contraction increases palmitate esterification and oxidation and triacylglycerol oxidation. The American Journal of Physiology. 1998;275(5 Part 1):E888–E896.

86. ^Peters S. J., Dyck D. J., Bonen A., Spriet L. L. Effects of epinephrine on lipid metabolism in resting skeletal muscle. The American Journal of Physiology. 1998;275(2 Part 1):E300–E309.

87. ^Dyck D. J., Bonen A. Muscle contraction increases palmitate esterification and oxidation and triacylglycerol oxidation. The American Journal of Physiology. 1998;275(5 Part 1):E888–E896.

88. ^alanian J.L., Tunstall R.J., Watt M.J., Duong M., Perry C.G.R., Steinberg G.R., Kemp B.E., Heigenhauser G.J.F., Spriet L.L. Adrenergic regulation of HSL serine phosphorylation and activity in human skeletal muscle during the onset of exercise. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2006;291:1094–1099.

89. ^Jocken J.W., Blaak E.E. Catecholamine-induced lipolysis in adipose tissue and skeletal muscle in obesity. Physiol. Behav. 2008;94:219–230.

90. ^Holm C., Osterlund T., Laurell H., Contreras J.A. Molecular mechanisms regulating hormone-sensitive lipase and lipolysis. Annu. Rev. Nutr. 2000;20:365–393.

91. ^Shen W.J., Patel S., Natu V., Kraemer F.B. Mutational analysis of structural features of rat hormone-sensitive lipase. Biochemistry. 1998;37:8973–8979.

92. ^Zimmermann R., Strauss J.G., Haemmerle G., Schoiswohl G., Birner-Gruenberger R., Riederer M., Lass A., Neuberger G., Eisenhaber F., Hermetter A., et al. Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase. Science. 2004;306:1383–1386.

93. ^Villena J.A., Roy S., Sarkadi-Nagy E., Kim K.H., Sul H.S. Desnutrin, an adipocyte gene encoding a novel patatin domain-containing protein, is induced by fasting and glucocorticoids: Ectopic expression of desnutrin increases triglyceride hydrolysis. J. Biol. Chem. 2004;279:47066–47075.

94. ^Roepstorff C., Vistisen B., Kiens B. Intramuscular triacylglycerol in energy metabolism during exercise in humans. Exerc. Sport Sci. Rev. 2005;33:182–188.

95. ^Vaughan M, Berger JE, Steinberg D 1964. Hormone-sensitive lipase and monoglyceride lipase activities in adipose tissue. J Biol Chem 239: 401–409

96. ^Petridou A., Chatzinikolaou A., Avloniti A., Jamurtas A., Loules G., Papassotiriou I., Fatouros I., Mougios V. Increased triacylglycerol lipase activity in adipose tissue of lean and obese men during endurance exercise. J. Clin. Endocrinol.

97. ^Jenkins CM, Mancuso DJ, Yan W, Sims HF, Gibson B, Gross RW 2004. Identification, cloning, expression, and purification of three novel human calcium-independent phospholipase A2 family members possessing triacylglycerol lipase and acylglycerol transacylase activities. J Biol Chem 279: 48968–48975

98. ^Zechner R, Kienesberger PC, Haemmerle G, Zimmermann R, Lass A 2009. Adipose triglyceride lipase and the lipolytic catabolism of cellular fat stores. J Lipid Res 50: 3–21

99. ^Zimmermann R, Strauss JG, Haemmerle G, Schoiswohl G, Birner-Gruenberger R, Riederer M, Lass A, Neuberger G, Eisenhaber F, Hermetter A, et al. 2004. Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase. Science 306: 1383–1386

100. ^Eichmann TO, Kumari M, Haas JT, Farese RV Jr, Zimmermann R, Lass A, Zechner R 2012. Studies on the substrate and stereo/regioselectivity of adipose triglyceride lipase, hormone-sensitive lipase, and diacylglycerol-O-acyltransferases. J Biol Chem 287: 41446–41457

101. ^Vaughan M, Berger JE, Steinberg D 1964. Hormone-sensitive lipase and monoglyceride lipase activities in adipose tissue. J Biol Chem 239: 401–409

102. ^Haemmerle G, Zimmermann R, Hayn M, Theussl C, Waeg G, Wagner E, Sattler W, Magin TM, Wagner EF, Zechner R 2002. Hormone-sensitive lipase deficiency in mice causes diglyceride accumulation in adipose tissue, muscle, and testis. J Biol Chem 277: 4806–4815

103. ^Schweiger M, Schreiber R, Haemmerle G, Lass A, Fledelius C, Jacobsen P, Tornqvist H, Zechner R, Zimmermann R 2006. Adipose triglyceride lipase and hormone-sensitive lipase are the major enzymes in adipose tissue triacylglycerol catabolism. J Biol Chem 281: 40236–40241

104. ^Morley N, Kuksis A 1972. Positional specificity of lipoprotein lipase. J Biol Chem 247: 6389–6393

105. ^ogalska E, Cudrey C, Ferrato F, Verger R 1993. Stereoselective hydrolysis of triglycerides by animal and microbial lipases. Chirality 5: 24–30

106. ^Bertrand T, Auge F, Houtmann J, Rak A, Vallee F, Mikol V, Berne PF, Michot N, Cheuret D, Hoornaert C, et al. 2010. Structural basis for human monoglyceride lipase inhibition. J Mol Biol 396: 663–673

107. ^Ranallo R.F., Rhodes E.C. Lipid metabolism during exercise. Sports Med. 1998;26:29–42.

108. ^Campbell J, Martucci AD, Green GR. Plasma albumin as an acceptor of free fatty acids. Biochem J. 1964;93:183–189.

109. ^Miller N.E. HDL metabolism and its role in lipid transport. Eur. Heart J. 1990;11:1–3.

110. ^Doege H, Stahl A. Protein-mediated fatty acid uptake: novel insights from in vivo models. Physiology (Bethesda) 2006;21:259–268.

111. ^Gimeno RE, Ortegon AM, Patel S, et al. Characterization of a heart-specific fatty acid transport protein. J Biol Chem. 2003;278:16039–16044.

112. ^Schaap FG, Binas B, Danneberg H, van der Vusse GJ, Glatz JF. Impaired long-chain fatty acid utilization by cardiac myocytes isolated from mice lacking the heart-type fatty acid binding protein gene. Circ Res. 1999;85:329–337.

113. ^Jeukendrup AE. Regulation of fat metabolism in skeletal muscle. Ann N Y Acad Sci. 2002;967:217–235.

114. ^Harasim E., Kalinowska A., Chabowski A., Stepek T. The role of fatty-acid transport proteins (FAT/CD36, FABPpm, FATP) in lipid metabolism in skeletal muscles. Postepy Higieny Medycyny Doswiadczalnej. 2008;62:433–441.

115. ^Bruce CR, Brolin C, Turner N, Cleasby ME, van der Leij FR, Cooney GJ, Kraegen EW. Overexpression of carnitine palmitoyltransferase I in skeletal muscle in vivo increases fatty acid oxidation and reduces triacylglycerol esterification. Am J Physiol Endocrinol Metab. 2007;292:E1231–1237.

116. ^Monaco C., Whitfield J., Jain S.S., Spriet L.L., Bonen A., Holloway G.P. Activation of AMPKα2 is not required for mitochondrial FAT/CD36 accumulation during exercise. PLoS ONE. 2015;10:e0126122.

117. ^van der Leij FR, Huijkman NC, Boomsma C, Kuipers JR, Bartelds B. Genomics of the human carnitine acyltransferase genes. Mol Genet Metab. 2000;71:139–153.

118. ^Bonnefont JP, Djouadi F, Prip-Buus C, Gobin S, Munnich A, Bastin J. Carnitine palmitoyltransferases 1 and 2: biochemical, molecular and medical aspects. Mol Aspects Med. 2004;25:495–520.

119. ^McGarry J.D., Brown N.F. The mitochondrial carnitine palmitoyltransferase system. Eur. J. Biochem. 1997;244:1–14.

120. ^Holloway G.P., Bezaire V., Heigenhauser G.J.F., Tandon N.N., Glatz J.F.C., Luiken J.J.F.P., Bonen A., Spriet L.L. Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise. J. Physiol. 2006;571:201–210.

121. ^Houten S.M., Violante S., Ventura F.V., Wanders R.J. The biochemistry and physiology of mitochondrial fatty acid β-oxidation and its genetic disorders. Annu. Rev. Physiol. 2016;78:23–44.