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Journal articles on the topic 'Fat metabolism'

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Published: 4 June 2021
Last updated: 5 March 2023

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1

Pei, Liming, and Ronald M. Evans. "Retrofitting Fat Metabolism." Cell Metabolism 9, no. 6 (June 2009): 483–84. http://dx.doi.org/10.1016/j.cmet.2009.05.006.

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2

Leslie, Eric, Christine Mermier, and Len Kravitz. "Exercise and Fat Metabolism." ACSM'S Health & Fitness Journal 26, no. 3 (May 2022): 34–39. http://dx.doi.org/10.1249/fit.0000000000000768.

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3

Landecker, Hannah. "Postindustrial Metabolism: Fat Knowledge." Public Culture 25, no. 3 (2013): 495–522. http://dx.doi.org/10.1215/08992363-2144625.

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4

Gleeson, Michael. "Basic metabolism I: fat." Surgery (Oxford) 23, no. 3 (March 2005): 83–88. http://dx.doi.org/10.1383/surg.23.3.83.63111.

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5

Samra, J. S., L. K. M. Summers, and K. N. Frayn. "Sepsis and fat metabolism." British Journal of Surgery 83, no. 9 (September 1996): 1186–96. http://dx.doi.org/10.1046/j.1365-2168.1996.02445.x.

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6

McAndrew, Philomena F. "Fat Metabolism and Cancer." Surgical Clinics of North America 66, no. 5 (October 1986): 1003–12. http://dx.doi.org/10.1016/s0039-6109(16)44037-5.

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7

Vogan, Kyle. "TM6SF2 and fat metabolism." Nature Genetics 46, no. 7 (June 26, 2014): 665. http://dx.doi.org/10.1038/ng.3023.

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8

Samra, J. S., L. K. M. Summers, and K. N. Frayn. "Sepsis and fat metabolism." British Journal of Surgery 83, no. 9 (September 1996): 1186–96. http://dx.doi.org/10.1002/bjs.1800830906.

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9

Jeukendrup, A. E., and R. Randell. "Fat burners: nutrition supplements that increase fat metabolism." Obesity Reviews 12, no. 10 (September 22, 2011): 841–51. http://dx.doi.org/10.1111/j.1467-789x.2011.00908.x.

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10

Egashira, Yukari, and Hiroo Sanada. "Dietary Fat and Tryptophan Metabolism." Nippon Eiyo Shokuryo Gakkaishi 55, no. 6 (2002): 357–60. http://dx.doi.org/10.4327/jsnfs.55.357.

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11

Moro, Cedric. "Natriuretic peptides and fat metabolism." Current Opinion in Clinical Nutrition and Metabolic Care 16, no. 6 (November 2013): 645–49. http://dx.doi.org/10.1097/mco.0b013e32836510ed.

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12

Campbell, P. J., M. G. Carlson, and N. Nurjhan. "Fat metabolism in human obesity." American Journal of Physiology-Endocrinology and Metabolism 266, no. 4 (April 1, 1994): E600—E605. http://dx.doi.org/10.1152/ajpendo.1994.266.4.e600.

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Excessive fat turnover and oxidation might cause the insulin resistance of carbohydrate metabolism in obese humans. We studied the response of free fatty acid (FFA) metabolism in lean and obese volunteers to sequential insulin infusions of 4, 8, 25, and 400 mU.m-2.min-1. The insulin dose-response curves for suppression of FFA concentration, FFA turnover ([1-14C]palmitate), and lipolysis ([2H5]glycerol) were shifted to the right in the obese subjects (insulin concentrations that produced a half-maximal response, lean vs. obese: 103 +/- 21 vs. 273 +/- 41, 96 +/- 11 vs. 264 +/- 44, and 101 +/- 23 vs. 266 +/- 44 pM, all P < 0.05), consistent with insulin resistance of FFA metabolism in obesity. After the overnight fast, FFA turnover per fat mass was decreased in obese subjects (37 +/- 4 vs. 20 +/- 3 mumol.kg fat mass-1.min-1, P < 0.01) as the result of suppression of lipolysis by the hyperinsulinemia of obesity and an increased fractional reesterification of FFA before leaving the adipocyte (primary FFA reesterification; 0.14 +/- 0.03 vs. 0.35 +/- 0.06, P < 0.05). Nevertheless, FFA turnover per fat-free mass (FFM) was also greater in the obese volunteers (8.5 +/- 0.7 vs. 11.0 +/- 1.0 mumol.kg FFM-1.min-1, P < 0.05) but only as the result of increased reesterification of intravascular FFA (secondary reesterification; 1.8 +/- 0.5 vs. 4.8 +/- 1.1 mumol.kg FFM-1.min-1, P < 0.01), since FFA oxidation was the same in the two groups throughout the insulin dose-response curve.(ABSTRACT TRUNCATED AT 250 WORDS)
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13

BJÖRNTORP, PER. "Fat Cell Distribution and Metabolism." Annals of the New York Academy of Sciences 499, no. 1 (December 17, 2006): 66–72. http://dx.doi.org/10.1111/j.1749-6632.1987.tb36198.x.

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14

&NA;. "Free Communication/Poster - Fat Metabolism." Medicine & Science in Sports & Exercise 40, Supplement (May 2008): 47. http://dx.doi.org/10.1249/01.mss.0000321008.13304.48.

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15

Blaak, Ellen. "Gender differences in fat metabolism." Current Opinion in Clinical Nutrition and Metabolic Care 4, no. 6 (November 2001): 499–502. http://dx.doi.org/10.1097/00075197-200111000-00006.

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16

Yip, Rupert G. C., and M. Michael Wolfe. "GIF biology and fat metabolism." Life Sciences 66, no. 2 (December 1999): 91–103. http://dx.doi.org/10.1016/s0024-3205(99)00314-8.

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17

Cray, S. "Fat metabolism during propofol infusion." British Journal of Anaesthesia 82, no. 3 (March 1999): 473. http://dx.doi.org/10.1093/bja/82.3.473.

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18

Machann, Jürgen, Andreas Fritsche, and Fritz Schick. "New Insights into Fat Metabolism." German Research 27, no. 3 (December 2005): 21–23. http://dx.doi.org/10.1002/germ.200590028.

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19

Gimble, Jeffrey M., and Z. Elizabeth Floyd. "Fat circadian biology." Journal of Applied Physiology 107, no. 5 (November 2009): 1629–37. http://dx.doi.org/10.1152/japplphysiol.00090.2009.

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While adipose tissue has long been recognized for its major role in metabolism, it is now appreciated as an endocrine organ. A growing body of literature has emerged that identifies circadian mechanisms as a critical regulator of adipose tissue differentiation, metabolism, and adipokine secretory function in both health and disease. This concise review focuses on recent data from murine and human models that highlights the interplay between the core circadian regulatory proteins and adipose tissue in the context of energy, fat, and glucose metabolism. It will be important to integrate circadian mechanisms and networks into future descriptions of adipose tissue physiology.
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20

Deitel, M. "It's a Fat, Fat, Fat, Fat World!" Obesity Surgery 14, no. 7 (August 1, 2004): 869–70. http://dx.doi.org/10.1381/0960892041719536.

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21

Corvera, Silvia. "Perinatal fat progenitors shape adult metabolism." Nature Metabolism 4, no. 8 (August 18, 2022): 963–64. http://dx.doi.org/10.1038/s42255-022-00626-5.

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22

Wang, Thomas J. "The Natriuretic Peptides and Fat Metabolism." New England Journal of Medicine 367, no. 4 (July 26, 2012): 377–78. http://dx.doi.org/10.1056/nejmcibr1204796.

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23

Carlson, Grant W. "The Breast, Fat, and Steroid Metabolism." Plastic and Reconstructive Surgery 123, no. 3 (March 2009): 117e—118e. http://dx.doi.org/10.1097/prs.0b013e31819a35db.

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24

"Internal Body Clock Controls Fat Metabolism." Asian Journal of Cell Biology 6, no. 1 (December 15, 2010): 24. http://dx.doi.org/10.3923/ajcb.2011.24.24.

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25

&NA;. "Free Communication/Slide - Fat Metabolism 1." Medicine & Science in Sports & Exercise 40, Supplement (May 2008): 36. http://dx.doi.org/10.1249/01.mss.0000320804.73699.a1.

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26

&NA;. "Free Communication/Slide - Fat Metabolism 2." Medicine & Science in Sports & Exercise 40, Supplement (May 2008): 51. http://dx.doi.org/10.1249/01.mss.0000321073.88564.ba.

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27

Wiener, Michael, Michael M. Rothkopf, Gail Rothkopf, and Jeffrey Askanazi. "Fat Metabolism in Injury and Stress." Critical Care Clinics 3, no. 1 (January 1987): 25–56. http://dx.doi.org/10.1016/s0749-0704(18)30560-8.

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28

Ranneries, Claudia, Jens Bülow, Benjamin Buemann, Niels Juel Christensen, Joop Madsen, and Arne Astrup. "Fat metabolism in formerly obese women." American Journal of Physiology-Endocrinology and Metabolism 274, no. 1 (January 1, 1998): E155—E161. http://dx.doi.org/10.1152/ajpendo.1998.274.1.e155.

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An impaired fat oxidation has been implicated to play a role in the etiology of obesity, but it is unclear to what extent impaired fat mobilization from adipose tissue or oxidation of fat is responsible. The present study aimed to examine fat mobilization from adipose tissue and whole body fat oxidation stimulated by exercise in seven formerly obese women (FO) and eight matched controls (C). Lipolysis in the periumbilical subcutaneous adipose tissue, whole body energy expenditure (EE), and substrate oxidation rates were measured before, during, and after a 60-min bicycle exercise bout of moderate intensity. Lipolysis was assessed by glycerol release using microdialysis and blood flow measurement by 133Xe clearance technique. The FO women had lower resting EE than C (3.77 ± 1.01 vs. 4.88 ± 0.74 kJ/min, P < 0.05) but responded similarly to exercise. Adipose tissue glycerol release was twice as high in FO than in C at rest (0.455 ± 0.299 vs. 0.206 ± 0.102 μmol ⋅ 100 g−1 ⋅ min−1, P < 0.05) but increased similarly in FO and C in response to exercise. Despite higher plasma nonesterified fatty acids (NEFA) in FO ( P < 0.001), fat oxidation rates during rest and recovery were lower in FO than in C (1.32 ± 0.84 vs. 3.70 ± 0.57 kJ/min, P < 0.02) and fat oxidation for a given plasma NEFA concentration was lower at rest ( P < 0.001) and during exercise ( P = 0.01) in the formerly obese group. In conclusion, fat mobilization both at rest and during exercise is intact in FO, whereas fat oxidation is subnormal despite higher circulation NEFA levels. The lower resting EE and the failure to use fat as fuel contribute to a positive fat balance and weight gain in FO subjects.
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29

Kim, Eun Ju, Yeon Kyung Kim, Ji Eun Kim, Sojeong Kim, Min-Kyoung Kim, Chi-Hyun Park, and Jin Ho Chung. "UV Modulation of Subcutaneous Fat Metabolism." Journal of Investigative Dermatology 131, no. 8 (August 2011): 1720–26. http://dx.doi.org/10.1038/jid.2011.106.

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30

Piché, Marie-Eve, and Paul Poirier. "Obesity, ectopic fat and cardiac metabolism." Expert Review of Endocrinology & Metabolism 13, no. 4 (July 4, 2018): 213–21. http://dx.doi.org/10.1080/17446651.2018.1500894.

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31

Loftus, Thomas M. "Introduction: Fat metabolism and adipose homeostasis." Seminars in Cell & Developmental Biology 10, no. 1 (February 1999): 1–2. http://dx.doi.org/10.1006/scdb.1998.0270.

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32

Hwang, S., LK Sarna, YL Siow, and K O. "High Fat Diet Disrupts Homocysteine Metabolism." Canadian Journal of Cardiology 29, no. 10 (October 2013): S168—S169. http://dx.doi.org/10.1016/j.cjca.2013.07.256.

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33

Lecka-Czernik, Beata. "Marrow fat metabolism is linked to the systemic energy metabolism." Bone 50, no. 2 (February 2012): 534–39. http://dx.doi.org/10.1016/j.bone.2011.06.032.

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34

Ko, Seong-Hee, and YunJae Jung. "Energy Metabolism Changes and Dysregulated Lipid Metabolism in Postmenopausal Women." Nutrients 13, no. 12 (December 20, 2021): 4556. http://dx.doi.org/10.3390/nu13124556.

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Aging women experience hormonal changes, such as decreased estrogen and increased circulating androgen, due to natural or surgical menopause. These hormonal changes make postmenopausal women vulnerable to body composition changes, muscle loss, and abdominal obesity; with a sedentary lifestyle, these changes affect overall energy expenditure and basal metabolic rate. In addition, fat redistribution due to hormonal changes leads to changes in body shape. In particular, increased bone marrow-derived adipocytes due to estrogen loss contribute to increased visceral fat in postmenopausal women. Enhanced visceral fat lipolysis by adipose tissue lipoprotein lipase triggers the production of excessive free fatty acids, causing insulin resistance and metabolic diseases. Because genes involved in β-oxidation are downregulated by estradiol loss, excess free fatty acids produced by lipolysis of visceral fat cannot be used appropriately as an energy source through β-oxidation. Moreover, aged women show increased adipogenesis due to upregulated expression of genes related to fat accumulation. As a result, the catabolism of ATP production associated with β-oxidation decreases, and metabolism associated with lipid synthesis increases. This review describes the changes in energy metabolism and lipid metabolic abnormalities that are the background of weight gain in postmenopausal women.
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35

Williams, Christine M. "Lipid metabolism in women." Proceedings of the Nutrition Society 63, no. 1 (February 2004): 153–60. http://dx.doi.org/10.1079/pns2003314.

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Differences in whole-body lipid metabolism between men and women are indicated by lower-body fat accumulation in women but more marked accumulation of fat in the intra-abdominal visceral fat depots of men. Circulating blood lipid concentrations also show gender-related differences. These differences are most marked in premenopausal women, in whom total cholesterol, LDL-cholesterol and triacylglycerol concentrations are lower and HDL-cholesterol concentration is higher than in men. Tendency to accumulate body fat in intra-abdominal fat stores is linked to increased risk of CVD, metabolic syndrome, diabetes and other insulin-resistant states. Differential regional regulation of adipose tissue lipolysis and lipogenesis must underlie gender-related differences in the tendency to accumulate fat in specific fat depots. However, empirical data to support current hypotheses remain limited at the present time because of the demanding and specialist nature of the methods used to study adipose tissue metabolism in human subjects. In vitro and in vivo data show greater lipolytic sensitivity of abdominal subcutaneous fat and lesser lipolytic sensitivity of femoral and gluteal subcutaneous fat in women than in men. These differences appear to be due to fewer inhibitory α adrenergic receptors in abdominal regions and greater α adrenergic receptors in gluteal and femoral regions in women than in men. There do not appear to be major gender-related differences in rates of fatty acid uptake (lipogenesis) in different subcutaneous adipose tissue regions. In visceral fat rates of both lipolysis and lipogenesis appear to be greater in men than in women; higher rates of lipolysis may be due to fewer α adrenergic receptors in this fat depot in men. Fatty acid uptake into this depot in the postprandial period is approximately 7-fold higher in men than in women. Triacylglycerol concentrations appear to be a stronger cardiovascular risk factor in women than in men, with particular implications for cardiovascular risk in diabetic women. The increased triacylglycerol concentrations observed in women taking hormone-replacement therapy (HRT) may explain the paradoxical findings of increased rates of CVD in women taking HRT that have been reported from recent primary and secondary prevention trials of HRT.
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36

Van Horn, Linda. "Metabolism: Assessment and Applications Vary by Fat and Fat-Free Mass." Journal of the American Dietetic Association 111, no. 11 (November 2011): 1641. http://dx.doi.org/10.1016/j.jada.2011.09.019.

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37

Li, M., D. Gu, N. Xu, F. Lei, L. Du, Y. Zhang, and W. Xie. "Gut carbohydrate metabolism instead of fat metabolism regulated by gut microbes mediates high-fat diet-induced obesity." Beneficial Microbes 5, no. 3 (September 1, 2014): 335–44. http://dx.doi.org/10.3920/bm2013.0071.

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The aim of this study was to investigate the mechanisms underlying the involvement of gut microbes in body weight gain of high-fat diet-fed obesity-prone (obese) and obesity-resistant (lean) mice. C57BL/6 mice were grouped into an obese group, a lean group and a normal control group. Both obese and lean mice were fed a high-fat diet while normal control mice were fed a normal diet; they were observed for six weeks. The results showed that lean mice had lower serum lipid levels, body fat and weight gain than obese mice. The ATPase, succinate dehydrogenase and malate dehydrogenase activities in liver as well as oxygen expenditure and rectal temperature of lean mice were significantly lower than in obese mice. As compared with obese mice, the absorption of intestinal carbohydrates but not of fats or proteins was significantly attenuated in lean mice. Furthermore, 16S rRNA abundances of faecal Firmicutes and Bacteroidetes were significantly reduced in lean mice. In addition, faecal β-D-galactosidase activity and short chain fatty acid levels were significantly decreased in lean mice. Expressions of peroxisome proliferator-activated receptor gamma 2 and CCAAT/enhancer binding protein-β in visceral adipose tissues were significantly downregulated in lean mice as compared with obese mice. Resistance to dyslipidaemia and high-fat diet-induced obesity was mediated by ineffective absorption of intestinal carbohydrates but not of fats or proteins, probably through reducing gut Bacteroidetes and Firmicutes contents and lowering of gut carbohydrate metabolism. The regulation of intestinal carbohydrates instead of fat absorption by gut microbes might be a potential treatment strategy for high-fat diet-induced obesity.
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38

Qureshi, Asjid, and Peter G. Kopelman. "Leptin - fat messenger or fat controller?" Clinical Endocrinology 47, no. 2 (August 1997): 169–71. http://dx.doi.org/10.1046/j.1365-2265.1997.2931092.x.

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39

Cardoso, Filipa. "The brain-fat connection." Science 378, no. 6619 (November 4, 2022): 485. http://dx.doi.org/10.1126/science.ade2132.

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40

FARNWORTH, E. R., and J. K. G. KRAMER. "FAT METABOLISM IN GROWING SWINE: A REVIEW." Canadian Journal of Animal Science 67, no. 2 (June 1, 1987): 301–18. http://dx.doi.org/10.4141/cjas87-029.

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At birth, piglets have little body fat that can be mobilized. The influx of high-fat milk causes a rapid increase in body fat stores and a depression of lipogenic enzyme activity. Conversely, lipolytic enzyme activity increases after birth. Changing the fat intake of sucking piglets affects the amount of fat deposition. The length of the sucking period also influences body composition at weaning. Weaning produces a pronounced but temporary decrease in total body lipid, despite an increase in fat synthesis. The effect of weaning on lipolysis is not clear due to a lack of experimental data. During the growing period, fat continues to build up even though lipogenic enzyme activity tends to decline with age. The composition of the diet, the sex of the animal and genetic factors have all been shown to influence the rate of lipogenesis. Fewer reports have been published in which factors affecting lipolysis have been studied and the results are often less conclusive. However, the combined activities of lipogenic and lipolytic processes do not account for the large quantity of body fat found in growing pigs. Key words: Swine, fat, lipogenesis, lipolysis, diet, sex.
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41

HONG, QIN, CHEN XIA, HU XIANGYING, and YUAN QUAN. "Capsinoids suppress fat accumulation via lipid metabolism." Molecular Medicine Reports 11, no. 3 (November 24, 2014): 1669–74. http://dx.doi.org/10.3892/mmr.2014.2996.

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42

Bloor, W. R. "FAT METABOLISM IN THE EARLY 1900'S." Nutrition Reviews 10, no. 7 (April 27, 2009): 193–95. http://dx.doi.org/10.1111/j.1753-4887.1952.tb01145.x.

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43

Romijn, J. A., E. F. Coyla, L. Sidossis, J. F. HoroWit, and R. R. Wolfe. "EFFECTS OF EXERCISE INTENSITY ON FAT METABOLISM." Medicine & Science in Sports & Exercise 24, Supplement (May 1992): S72. http://dx.doi.org/10.1249/00005768-199205001-00432.

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44

Friedman, M. I., and I. Ramirez. "Relationship of fat metabolism to food intake." American Journal of Clinical Nutrition 42, no. 5 (November 1, 1985): 1093–98. http://dx.doi.org/10.1093/ajcn/42.5.1093.

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45

JEUKENDRUP, ASKER E. "Regulation of Fat Metabolism in Skeletal Muscle." Annals of the New York Academy of Sciences 967, no. 1 (January 24, 2006): 217–35. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04278.x.

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46

Crockett, Claude H. "Fat Metabolism and the Physiology of Liposuction." American Journal of Cosmetic Surgery 23, no. 1 (March 2006): 5–8. http://dx.doi.org/10.1177/074880680602300102.

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47

Cree, Melanie G., and Robert R. Wolfe. "Postburn trauma insulin resistance and fat metabolism." American Journal of Physiology-Endocrinology and Metabolism 294, no. 1 (January 2008): E1—E9. http://dx.doi.org/10.1152/ajpendo.00562.2007.

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Hyperglycemia and insulin resistance have long been recognized in severe burn patients. More recently, it has been observed that controlling hyperglycemia, or alleviating insulin resistance, is associated with improved outcomes. This has led to a renewed interest in the etiology of insulin resistance in this population. The postinjury hyperglycemic response appears to be associated with multiple metabolic abnormalities, such as elevated basal energy expenditure, increased protein catabolism, and, notably, significant alterations in fat metabolism. The synergy of all of the responses is not understood, although many studies have been conducted. In this article we will review the present understanding of the relationship between fat metabolism and insulin resistance posttrauma, and discuss some of the recent discoveries and potential therapeutic measures. We propose that the insulin resistance is likely related to the development of “ectopic” fat stores, i.e., triglyceride (TG) storage in sites such as the liver and muscle cells. Deposition of TG in ectopic sites is due to an increase in free fatty acid delivery secondary to catecholamine-induced lipolysis, in conjunction with decreased β-oxidation within muscle and decreased hepatic secretion of fats. The resultant increases in intracellular TG or related lipid products may in turn contribute to alterations in insulin signaling.
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48

Flatt, J. P. "Body Weight, Fat Storage, and Alcohol Metabolism." Nutrition Reviews 50, no. 9 (April 27, 2009): 267–70. http://dx.doi.org/10.1111/j.1753-4887.1992.tb01344.x.

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49

Laurencikiene, J., and M. Rydén. "Liver X receptors and fat cell metabolism." International Journal of Obesity 36, no. 12 (February 28, 2012): 1494–502. http://dx.doi.org/10.1038/ijo.2012.21.

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50

Rosania, Kara. "Viewing fat in zebrafish to study metabolism." Lab Animal 41, no. 8 (July 20, 2012): 209. http://dx.doi.org/10.1038/laban0812-209a.

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