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Glycerine – Claims vs. Facts

 
An ingredient in some of the most popular protein bars on the market today is a key ingredient in your soap….
©Ori Hofmekler

Glycerine (also known as glycerol) is a sugar alcohol substance with a syrupy texture and a slightly sweet alcoholic taste, commonly used as a filler in the manufacturing of low carb protein bars as well as in low fat baking goods and ice creams. Glycerine seems to make low carb products more appealing texture wise. It has also been used as a laxative and as an ingredient in pharmaceutical tinctures, soaps, electronic cigarettes and antifreeze.

 

Claims….

Glycerine has been claimed to promote weight loss, enhance athletic performance and improve hydration.

Facts:

  • Glycerine has the same calorie count as sugar.
  • The body uses glycerine for the synthesis of triglycerides (fatty acids) which are deposited as fat storage
  • Storage of excess triglycerides is central to obesity
  • Glycerine can convert into glucose (via gluconeogenesis) and thus inhibit ketosis
  • Inhibition of the process that converts glycerine to triglycerides have shown to decrease body weight, increase insulin sensitivity, inhibit fat gain (suppress lipogenic enzymes) and prevent the accumulation of lipids in liver and adipose (fat storing) tissues in animal models.
  • Glycerine is typically derived from soy/palm oil or animals tallow.
  • Glycerine can cause bloating and laxative side effects.

 

Effectiveness

  • Oral glycerine does not seem to promote weight loss in humans
  • Glycerine does not seem to improve athletic performance or hydration.
  • Glycerine inhibits Ketosis.

Notes

Glycerine should be treated like sugar alcohol and thus should be generally restricted except for cases where it’s used as an alcohol replacement in pharmaceutical products such as in tinctures, cough syrups or mouthwashes. Being anti-ketogenic, glycerine should be avoided by individuals on a ketogenic diet.

 

 

References

 Bell RM, Coleman RA. Enzymes of glycerolipid synthesis in eukaryotes. Annu Rev Biochem 49: 459–487, 1980

Choi SS, Diehl AM. Hepatic triglyceride synthesis and nonalcoholic fatty liver disease. Curr Opin Lipidol 19: 295–300, 2008

Coleman RA, Lewin TM, Muoio DM. Physiological and nutritional regulation of enzymes of triacylglycerol synthesis. Annu Rev Nutr 20: 77–103, 2000

Enriori PJ, Evans AE, Sinnayah P, Jobst EE, Tonelli-Lemos L, Billes SK, Glavas MM, Grayson BE, Perello M, Nillni EA, Grove KL, Cowley MA. Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons. Cell Metab 5: 181–194, 2007

Gimeno RE, Cao J. Thematic review series: glycerolipids. Mammalian glycerol-3-phosphate acyltransferases: new genes for an old activity. J Lipid Res 49: 2079–2088, 2008

Hammond LE, Gallagher PA, Wang S, Hiller S, Kluckman KD, Posey-Marcos EL, Maeda N, Coleman RA. Mitochondrial glycerol-3-phosphate acyltransferase-deficient mice have reduced weight and liver triacylglycerol content and altered glycerolipid fatty acid composition. Mol Cell Biol 22: 8204–8214, 2002

Kotronen A, Yki-Jarvinen H. Fatty liver: a novel component of the metabolic syndrome. Arterioscler Thromb Vasc Biol 28: 27–38, 2008

Kuhajda FP, Jenner K, Wood FD, Hennigar RA, Jacobs LB, Dick JD, Pasternack GR. Fatty acid synthesis: a potential selective target for antineoplastic therapy. Proc Natl Acad Sci USA 91: 6379–6383, 1994

Lewin TM, Granger DA, Kim JH, Coleman RA. Regulation of mitochondrial sn-glycerol-3-phosphate acyltransferase activity: response to feeding status is unique in various rat tissues and is discordant with protein expression. Arch Biochem Biophys 396: 119–127, 2001

Linden D, William-Olsson L, Ahnmark A, Ekroos K, Hallberg C, Sjogren HP, Becker B, Svensson L, Clapham JC, Oscarsson J, Schreyer S. Liver-directed overexpression of mitochondrial glycerol-3-phosphate acyltransferase results in hepatic steatosis, increased triacylglycerol secretion and reduced fatty acid oxidation. FASEB J 20: 434–443, 2006

Loftus TM, Jaworsky DE, Frehywot GL, Townsend CA, Ronnett GV, Lane MD, Kuhajda FP. Reduced food intake and body weight in mice treated with fatty acid synthase inhibitors. Science 288: 2379–2381, 2000

Nagle CA, Klett EL, Coleman RA. Hepatic triacylglycerol accumulation and insulin resistance. J Lipid Res 50 Suppl: S74–S79, 2009

Rosen ED, Sarraf P, Troy AE, Bradwin G, Moore K, Milstone DS, Spiegelman BM, Mortensen RM.PPAR gamma is required for the differentiation of adipose tissue in vivo and in vitro. Mol Cell 4: 611–617, 1999

Samuel VT, Petersen KF, Shulman GI. Lipid-induced insulin resistance: unravelling the mechanism.Lancet 375: 2267–2277, 2010

Thuresson ER. Inhibition of glycerol-3-phosphate acyltransferase as a potential treatment for insulin resistance and type 2 diabetes. Curr Opin Investig Drugs 5: 411–418, 2004

About Ori Hofmekler — founder of Defense Nutrition and author of The Warrior Diet, is a nutritional and fitness expert. Follow him on Twitter, Facebook and Google+.