Sucralose in Supplements: The hidden “filler” that threatens your health?
By Dr. Dwayne N. Jackson, PhD
Does the supplement company you support use artificial chemical sweeteners? It’s easy to tell, you can look at the label, or just evaluate taste. Be honest, does your favorite preworkout, intraworkout, or postworkout supplements taste like sweet candy? Although flavor is one easy way to decide your favorite brand, I want to enlighten you on a big supplement formulation secret. Large doses of artificial sweeteners like sucralose and ACE-K are being pumped into supplements simply because these cheap and make flavoring easier—but, most of all, they make great hidden fillers and increase profit margins. If you use a sucralose sweetened supplement, serving for serving, you sacrifice a proportion of your active ingredients for cheap sweetener. Even more importantly, by ingesting the large amounts of sucralose found in chemically sweetened supplements, you are detracting from your gains in performance and health. If you haveIIIf IIIIISucrolose in your supplements? Supplement companies are slowly damaging your health to protect their bottom line. TheTtttttis a synthetic organochlorine sweetener (OC) that is a common ingredient in the world's food supply. Sucralose interacts with chemosensors in the alimentary tract that play a role in sweet taste sensation and hormone secretion. In rats, sucralose ingestion was shown to increase the expression of the efflux transporter P-glycoprotein (P-gp) and two cytochrome P-450 (CYP) isozymes in the intestine. P-gp and CYP are key components of the presystemic detoxification system involved in first-pass drug metabolism. The effect of sucralose on first-pass drug metabolism in humans, however, has not yet been determined. In rats, sucralose alters the microbial composition in the gastrointestinal tract (GIT), with relatively greater reduction in beneficial bacteria. Although early studies asserted that sucralose passes through the GIT unchanged, subsequent analysis suggested that some of the ingested sweetener is metabolized in the GIT, as indicated by multiple peaks found in thin-layer radiochromatographic profiles of methanolic fecal extracts after oral sucralose administration. The identity and safety profile of these putative sucralose metabolites are not known at this time. Sucralose and one of its hydrolysis products were found to be mutagenic at elevated concentrations in several testing methods. Cooking with sucralose at high temperatures was reported to generate chloropropanols, a potentially toxic class of compounds. Both human and rodent studies demonstrated that sucralose may alter glucose, insulin, and glucagon-like peptide 1 (GLP-1) levels. Taken together, these findings indicate that sucralose is not a biologically inert compound.Sucralose is a synthetic organochlorine sweetener (OC) that is a common ingredient in the world's food supply. Sucralose interacts with chemosensors in the alimentary tract that play a role in sweet taste sensation and hormone secretion. In rats, sucralose ingestion was shown to increase the expression of the efflux transporter P-glycoprotein (P-gp) and two cytochrome P-450 (CYP) isozymes in the intestine. P-gp and CYP are key components of the presystemic detoxification system involved in first-pass drug metabolism. The effect of sucralose on first-pass drug metabolism in humans, however, has not yet been determined. In rats, sucralose alters the microbial composition in the gastrointestinal tract (GIT), with relatively greater reduction in beneficial bacteria. Although early studies asserted that sucralose passes through the GIT unchanged, subsequent analysis suggested that some of the ingested sweetener is metabolized in the GIT, as indicated by multiple peaks found in thin-layer radiochromatographic profiles of methanolic fecal extracts after oral sucralose administration. The identity and safety profile of these putative sucralose metabolites are not known at this time. Sucralose and one of its hydrolysis products were found to be mutagenic at elevated concentrations in several testing methods. Cooking with sucralose at high temperatures was reported to generate chloropropanols, a potentially toxic class of compounds. Both human and rodent studies demonstrated that sucralose may alter glucose, insulin, and glucagon-like peptide 1 (GLP-1) levels. Taken together, these findings indicate that sucralose is not a biologically inert compound. been led to believe that sucralose is a healthy calorie free sweetener, you are not alone--- after all, sucralose is made from sugar and has no calories. Sucralose is produced from sucrose (table sugar) by chemically replacing its hydrogen-oxygen groups for chlorine atom.
Seems harmless, right? This chemical processing of sugar increases its sweetness 600x and eliminates its caloric load, which has misled the public to equate sucralose use with health. However, we now know that although sucralose is calorie free and very sweet, it actions in your body are far from “healthy”. Sucralose is considered a synthetic organochlorine sweetener (OC), which has become a major ingredient in the world's food chain. Sucralose interacts with chemosensors in the digestive tract that play a role in sweet taste sensation and hormone secretion. Early studies claimed that sucralose passes through the gastrointestinal tract unaltered---suggesting that it is not metabolized. It was these past studies that led us to believe sucralose was harmless and healthy. However, contrary to early reports, recent science illustrates that about 15% of ingested sucralose is digested and metabolized, producing different compounds in the body which impact can health. So, the more sucralose you take in, the greater the potential impact these sucralose metabolites. In the grand scheme, although a diet soda here and there may not show up on your health charts, chronic ingestion of large amounts of chemical sweeteners, like sucralose, will likely have a negative impact on your overall health down the road.
In recent years, the unnecessary addition of large amounts of sucralose and artificial sweeteners in fitness supplements has become epidemic. That’s right, under the guise of health and taste, chemical sweeteners are being added to most products simply as “tasty hidden fillers”. In a review published in The Journal of Toxicology and Environmental Health, several health concerns of sucralose were raised:
  1. Sucralose and one of its metabolic by-products were found to increase genetic mutations at elevated concentrations in several testing methods. You want to avoid mutagenic compounds, as they are initiators to diseases like cancer.
  2. Cooking with sucralose was reported produce compounds called chloropropanols, a potentially toxic class of compounds that are also linked to cancers and other alterations in biological processes.
  3. Sucralose has been shown to negatively impact gut flora and gut health by decreasing the number of healthy bacteria. Sucralose also modifies glucose handling through initiating insulin spikes and affecting glucagon-like peptide 1 (GLP-1) levels. This can be a major issue for those who engage in intermittent fasting for fat loss or in overweight individuals who are insulin insensitive or glucose intolerant.

Taken together, the above summary of findings indicate that sucralose is not the biologically inert compound we once thought it was.
Why are most supplement companies still using chemical sweeteners? Well, simply because chemical sweeteners are much cheaper and easier to flavor products with than the organic healthy alternatives like Stevia. Here’s the skinny:
FORMULATOR’S COST (per kilogram) FOR COMMON SWEETNERS IN FOUND YOUR SUPPLEMENTS ACE-K: $4.80 ASPARTAME: $6.20 ATP LAB’s Organic GMO Free Stevia: $200.00
That’s right! It costs 3000% to 4000% percent more to sweeten your products with healthy stevia! So, no wonder companies who still use chemical sweeteners tout the largest scoops and greatest taste.
At ATP LAB we use only organic non-GMO stevia in our products and since it’s so much more expensive than unhealthy chemical alternatives, we obviously use only what’s needed for taste. So, when comparing our products to others---gram for gram, you get less filler and more active ingredient. In the end, with ATP LAB supplements you get what you pay for---efficacious nutraceuticals, without detriment to your health.
    References: Schiffman SS, Rother KI. Sucralose, a synthetic organochlorine sweetener: overview of biological issues. J Toxicol Environ Health B Crit Rev. 2013;16(7):399-451. Abou-Donia M. B., Menzel D. B. Chick microsomal oxidases. Isolation, properties, and stimulation by embryonic exposure to 1,1,1-trichloro-2,2-bis(p chlorophenyl)ethane. Biochemistry. 1968a;7:3788–3794.  [PubMed] Abou-Donia M. B., Menzel D. B. The metabolism in vivo of 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane (DDD) and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) in the chick by embryonic injection and dietary ingestion. Biochem. Pharmacol. 1968b;17:2143–2161.  [PubMed] Abou-Donia M. B., El-Masry E. M., Abdel-Rahman A. A., McLendon R. E., Schiffman S. S. Splenda alters gut microflora and increases intestinal P-glycoprotein and cytochrome P-450 in male rats. J. Toxicol. Environ. Health A. 2008;71:1415–1429.  [PubMed] Abu-Qare A. W., Elmasry E., Abou-Donia M. B. A role for P-glycoprotein in environmental toxicology. J. Toxicol. Environ. Health B. 2003;6:279–288.  [PubMed] Adachi Y., Suzuki H., Sugiyama Y. Comparative studies on in vitro methods for evaluating in vivofunction of MDR1 P-glycoprotein. Pharm. Res. 2001;18:1660–1668.  [PubMed] Adas F., Berthou F., Picart D., Lozac'h P., Beaugé F., Amet Y. Involvement of cytochrome P450 2E1 in the (ω-1)-hydroxylation of oleic acid in human and rat liver microsomes. J. Lipid Res. 1998;39:1210–1219.  [PubMed] Aiba T., Takehara Y., Okuno M., Hashimoto Y. Poor correlation between intestinal and hepatic metabolic rates of CYP3A4 substrates in rats. Pharm. Res. 2003;20:745–748.  [PubMed] Albert M. J., Mathan V. I., Baker S. J. Vitamin B12 synthesis by human small intestinal bacteria. Nature. 1980;283:781–782.  [PubMed] Anderson E. S. The problem and implications of chloramphenicol resistance in the typhoid bacillus. J. Hyg. (Lond). 1975;74:289–299. [PMC free article]  [PubMed] Anderson G. H., Catherine N. L., Woodend D. M., Wolever T. M. Inverse association between the effect of carbohydrates on blood glucose and subsequent short-term food intake in young men. Am. J. Clin. Nutr. 2002;76:1023–1030.  [PubMed] Anderson M., Opawale F., Rao M., Delmarre D., Anyarambhatla G. Excipients for oral liquid formulations. In: Katdare A., Chaubal M. V., editors. Excipient development for pharmaceutical biotechnology, and drug delivery systems. New York, NY: Informa Healthcare USA; 2006. pp. 155–180. Anway M. D., Cupp A. S., Uzumcu M., Skinner M. K. Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science. 2005;308:1466–1469.  [PubMed] Aronson K. J., Miller A. B., Woolcott C. G., Sterns E. E., McCready D. R., Lickley L. A., Fish E. B., Hiraki G. Y., Holloway C., Ross T., Hanna W. M., SenGupta S. K., Weber J. P. Breast adipose tissue concentrations of polychlorinated biphenyls and other organochlorines and breast cancer risk. Cancer Epidemiol. Biomarkers Prev. 2000;9:55–63.  [PubMed] Backman J. T., Olkkola K. T., Neuvonen P. J. Rifampin drastically reduces plasma concentrations and effects of oral midazolam. Clin. Pharmacol. Ther. 1996;59:7–13.  [PubMed] Bae W., Mehra R. K., Mulchandani A., Chen W. Genetic engineering of Escherichia coli for enhanced uptake and bioaccumulation of mercury. Appl. Environ Microbiol. 2001;67:5335–5338.[PMC free article]  [PubMed] Bain L. J., LeBlanc G.A. Interaction of structurally diverse pesticides with the human MDR1 gene product P-glycoprotein. Toxicol. Appl. Pharmacol. 1996;141:288–298.  [PubMed] Baird I. M., Shephard N. W., Merritt R. J., Hildick-Smith G. Repeated dose study of sucralose tolerance in human subjects. Food Chem. Toxicol. 2000;38(suppl. 2):S123–S129.  [PubMed] Bannach G., Almeida R. R., Lacerda L. G., Schnitzler E., Ionashiro M. Thermal stability and thermal decomposition of sucralose. Ecl. Quím. São Paulo. 2009;34:21–26. Bapiro T. E., Egnell A. C., Hasler J. A., Masimirembwa C. M. Application of higher throughput screening (HTS) inhibition assays to evaluate the interaction of antiparasitic drugs with cytochrome P450s. Drug Metab. Dispos. 2001;29:30–35.  [PubMed] Barndt R. L., Jackson G. Stability of sucralose in baked goods. Food Technol. 1990;44(Jan):62–66. Bauer S., Störmer E., Johne A., Krüger H., Budde K., Neumayer H. H., Roots I., Mai I. Alterations in cyclosporin A pharmacokinetics and metabolism during treatment with St John's wort in renal transplant patients. Br. J. Clin. Pharmacol. 2003;55:203–211. [PMC free article]  [PubMed] Bauer T. M. The role of gut bacteria in drug metabolism. In: Blum H. E., Bode C., Bode J. C., Sartor R. B., editors. Gut and the liver. Hingham, MA: Kluwer Academic; 1998. pp. 177–184. Baumhäkel M., Kasel D., Rao-Schymanski R. A., Böcker R., Beckurts K. T., Zaigler M., Barthold D., Fuhr U. Screening for inhibitory effects of antineoplastic agents on CYP3A4 in human microsomes. Int. J. Clin. Pharmacol. Ther. 2001;39:517–528.  [PubMed] Baune B., Flinois J. P., Furlan V., Gimenez F., Taburet A. M., Becquemont L., Farinotti R. Halofantrine metabolism in microsomes in man: Major role of CYP 3A4 and CYP 3A5. J. Pharm. Pharmacol. 1999;51:419–426.  [PubMed] Becquemont L., Mouajjah S., Escaffre O., Beaune P., Funck-Brentano C., Jaillon P. Cytochrome P-450 3A4 and 2C8 are involved in zopiclone metabolism. Drug Metab. Dispos. 1999;27:1068–1073.[PubMed] Benet L. Z., Izumi T., Zhang Y., Silverman J. A., Wacher V. J. Intestinal MDR transport proteins and P-450 enzymes as barriers to oral drug delivery. J. Control Release. 1999;62:25–31.  [PubMed] Benet L. Z. The drug transportermetabolism alliance: Uncovering and defining the interplay. Mol. Pharm. 2009;6:1631–1643. [PMC free article]  [PubMed] Bennett C., Dordick J. S., Hacking A. J., Cheetham P. S. J. Biocatalytic synthesis of disaccharide high-intensity sweetener sucralose via a tetrachlororaffinose intermediate. Biotechnol. Bioeng. 1992;39:211–217.  [PubMed] Beringer P. M., Slaughter R. L. Transporters and their impact on drug disposition. Ann. Pharmacother. 2005;39:1097–1108.  [PubMed] Berson A., Descatoire V., Sutton A., Fau D., Maulny B., Vadrot N., Feldmann G., Berthon B., Tordjmann T., Pessayre D. Toxicity of alpidem, a peripheral benzodiazepine receptor ligand, but not zolpidem, in rat hepatocytes: Role of mitochondrial permeability transition and metabolic activation. J. Pharmacol. Exp. Ther. 2001;299:793–800.  [PubMed] Berthou F., Dreano Y., Belloc C., Kangas L., Gautier J. C., Beaune P. Involvement of cytochrome P450 3A enzyme family in the major metabolic pathways of toremifene in human liver microsomes. Biochem. Pharmacol. 1994;47:1883–1895.  [PubMed] Bertilsson L., Höjer B., Tybring G., Osterloh J., Rane A. Autoinduction of carbamazepine metabolism in children examined by a stable isotope technique. Clin. Pharmacol. Ther. 1980;27:83–88.  [PubMed] Bertilsson L., Tomson T., Tybring G. Pharmacokinetics: Time-dependent changes—Autoinduction of carbamazepine epoxidation. J. Clin. Pharmacol. 1986;26:459–462.  [PubMed] Biles R. W., Piper C. E. Mutagenicity of chloropropanol in a genetic screening battery. Fundam. Appl. Toxicol. 1983;3:27–33.  [PubMed] Birnbaum L. S. When environmental chemicals act like uncontrolled medicine. Trends Endocrinol. Metab. 2013;24:321–323.  [PubMed] Björkholm B., Bok C. M., Lundin A., Rafter J., Hibberd M. L., Pettersson S. Intestinal microbiota regulate xenobiotic metabolism in the liver. PLoS One. 2009;4:e6958. [PMC free article]  [PubMed] Blaser M. J., Falkow S. What are the consequences of the disappearing human microbiota? Nat. Rev. Microbiol. 2009;7:887–894.  [PubMed] Bogaards J. J., van Ommen B., Wolf C. R., van Bladeren P. J. Human cytochrome P450 enzyme selectivities in the oxidation of chlorinated benzenes. Toxicol. Appl. Pharmacol. 1995;132:44–52.[PubMed] Bonnet U. Moclobemide: Therapeutic use and clinical studies. CNS Drug Rev. 2003;9:97–140.[PubMed] Booth D. A.  Psychology of nutrition. London, UK: Taylor & Francis; 1994. pp. 56–57. Borchers A. T., Selmi C., Meyers F. J., Keen C. L., Gershwin M. E. Probiotics and immunity. J. Gastroenterol. 2009;44:26–46.  [PubMed] Bort R., Macé K., Boobis A., Gómez-Lechón M. J., Pfeifer A., Castell J. Hepatic metabolism of diclofenac: Role of human CYP in the minor oxidative pathways. Biochem. Pharmacol. 1999;58:787–796.  [PubMed] Bort R., Ponsoda X., Carrasco E., Gómez-Lechón M. J., Castell J. V. Metabolism of aceclofenac in humans. Drug Metab. Dispos. 1996;24:834–841.  [PubMed] Boulton D. W., DeVane C. L., Liston H. L., Markowitz J. S. In vitro P-glycoprotein affinity for atypical and conventional antipsychotics. Life Sci. 2002;71:163–169.  [PubMed] Brannan M. D., Affrime M. B., Radwanski E., Cayen M. N., Banfield C. Effects of various cytochrome P450 inhibitors on the metabolism of loratadine. Clin. Pharmacol. Ther. 1995;57:193. (OII-A-4). Brown A. W., Bohan Brown M. M., Onken K. L., Beitz D. C. Short-term consumption of sucralose, a nonnutritive sweetener, is similar to water with regard to select markers of hunger signaling and short-term glucose homeostasis in women. Nutr. Res. 2011;31:882–888.  [PubMed] Brown R. J., Rother K. I. Nonnutritive sweeteners and their role in the gastrointestinal tract. J. Clin. Endocrinol. Metab. 2012;97:2597–2605. [PMC free article]  [PubMed] Brown R. J., Walter M., Rother K. I. Ingestion of diet soda before a glucose load augments glucagon-like peptide-1 secretion. Diabetes Care. 2009;32:2184–2186. [PMC free article]  [PubMed] Brown R. J., Walter M., Rother K. I. Effects of diet soda on gut hormones in youths with diabetes. Diabetes Care. 2012;35:959–964. [PMC free article]  [PubMed] Brownlee K. A.  Statistical theory and methodology in science and engineering. New York, NY: John Wiley & Sons; 1960. Brusick D., Borzelleca J. F., Gallo M., Williams G., Kille J., Hayes A. W., Pi-Sunyer F. X., Williams C., Burks W. Expert panel report on a study of Splenda in male rats. Regul. Toxicol. Pharmacol. 2009;55:6–12.  [PubMed] Bruyère A., Declevès X., Bouzom F., Proust L., Martinet M., Walther B., Parmentier Y. Development of an optimized procedure for the preparation of rat intestinal microsomes: Comparison of hepatic and intestinal microsomal cytochrome P450 enzyme activities in two rat strains. Xenobiotica. 2009;39:22–32.  [PubMed] Burdge G. C., Hanson M. A., Slater-Jefferies J. L., Lillycrop K. A. Epigenetic regulation of transcription: A mechanism for inducing variations in phenotype (fetal programming) by differences in nutrition during early life? Br. J. Nutr. 2007;97:1036–1046. [PMC free article]  [PubMed] Cabrini L., Landi L., Stefanelli C., Barzanti V., Sechi A.M. Extraction of lipids and lipophilic antioxidants from fish tissues: A comparison among different methods. Comp. Biochem. Physiol. Part B. 1992;101:383–386.  [PubMed] Calafat A. M., Ye X., Wong L. Y., Reidy J. A., Needham L. L. Urinary concentrations of triclosan in the U.S. population: 2003–2004. Environ. Health Perspect. 2008;116:303–307. [PMC free article][PubMed] Chadwick R. W., Cooper R. L., Chang J., Rehnberg G. L., McElroy W. K. Possible antiestrogenic activity of lindane in female rats. J. Biochem. Toxicol. 1988;3:147–158.  [PubMed] Chang T. K., Yu L., Maurel P., Waxman D. J. Enhanced cyclophosphamide and ifosfamide activation in primary human hepatocyte cultures: Response to cytochrome P-450 inducers and autoinduction by oxazaphosphorines. Cancer Res. 1997;57:1946–1954.  [PubMed] Chen C., Hanson E., Watson J. W., Lee J. S. P-glycoprotein limits the brain penetration of nonsedating but not sedating H1-antagonists. Drug Metab. Dispos. 2003a;31:312–318.  [PubMed] Chen C., Staudinger J. L., Klaassen C. D. Nuclear receptor, pregname X receptor, is required for induction of UDP-glucuronosyltranferases in mouse liver by pregnenolone-16 alpha-carbonitrile. Drug Metab. Dispos. 2003b;31:908–915.  [PubMed] Chen J., Raymond K. Roles of rifampicin in drug-drug interactions: Underlying molecular mechanisms involving the nuclear pregnane X receptor. Ann. Clin. Microbiol. Antimicrob. 2006;5:3.[PMC free article]  [PubMed] Chen Y., Tang Y., Guo C., Wang J., Boral D., Nie D. Nuclear receptors in the multidrug resistance through the regulation of drug-metabolizing enzymes and drug transporters. Biochem. Pharmacol. 2012;83:1112–1126. [PMC free article]  [PubMed] Cho I., Blaser M. J. The human microbiome: At the interface of health and disease. Nat. Rev. Genet. 2012;13:260–270. [PMC free article]  [PubMed] Cho W. S., Han B. S., Lee H., Kim C., Nam K. T., Park K., Choi M., Kim S. J., Kim S. H., Jeong J., Jang D. D. Subchronic toxicity study of 3-monochloropropane-1,2-diol administered by drinking water to B6C3F1 mice. Food Chem. Toxicol. 2008;46:1666–1673.  [PubMed] Chonan O., Takahashi R., Watanuki M. Role of activity of gastrointestinal microflora in absorption of calcium and magnesium in rats fed ß1–4 linked galactooligosaccharides. Biosci. Biotechnol. Biochem. 2001;65:1872–1875.  [PubMed] Choo E. F., Leake B., Wandel C., Imamura H., Wood A. J., Wilkinson G. R., Kim R. B. Pharmacological inhibition of P-glycoprotein transport enhances the distribution of HIV-1 protease inhibitors into brain and testes. Drug Metab. Dispos. 2000;28:655–660.  [PubMed] Cizza G., Rother K. I. Beyond fast food and slow motion: Weighty contributors to the obesity epidemic. J. Endocrinol. Invest. 2012;35:236–242. [PMC free article]  [PubMed] Claus S. P., Tsang T. M., Wang Y., Cloarec O., Skordi E., Martin F. P., Rezzi S., Ross A., Kochhar S., Holmes E., Nicholson J. K. Systemic multicompartmental effects of the gut microbiome on mouse metabolic phenotypes. Mol. Syst. Biol. 2008;4:219. [PMC free article]  [PubMed] Clement B., Demesmaeker M. Formation of guanoxabenz from guanabenz in human liver. A new metabolic marker for CYP1A2. Drug Metab. Dispos. 1997;25:1266–1271.  [PubMed] Clemente J. C., Ursell L. K., Parfrey L. W., Knight R. The impact of the gut microbiota on human health: An integrative view. Cell. 2012;148:1258–1270. [PMC free article]  [PubMed] Colditz G. A., Willett W. C., Stampfer M. J., London S. J., Segal M. R., Speizer F. E. Patterns of weight change and their relation to diet in a cohort of healthy women. Am. J. Clin. Nutr. 1990;51:1100–1105.  [PubMed] Coleman S., Linderman R., Hodgson E., Rose R. L. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Environ. Health Perspect. 2000;108:1151–1157. [PMC free article]  [PubMed] Corkey B. E. Banting lecture 2011: Hyperinsulinemia: Cause or consequence? Diabetes. 2012;61:4–13.[PMC free article]  [PubMed] Coumoul X., Diry M., Barouki R. PXR-dependent induction of human CYP3A4 gene expression by organochlorine pesticides. Biochem. Pharmacol. 2002;64:1513–1519.  [PubMed] Crabbe E., Nolasco-Hipolito C., Kobayashi G., Sonomoto K., Ishizaki A. Biodiesel production from crude palm oil and evaluation of butanol extraction and fuel properties. Process Biochem. 2001;37:65–71. Cummings J. H., Macfarlane G. T. The control and consequences of bacterial fermentation in the human colon. J. Appl. Bacteriol. 1991;70:443–459.  [PubMed] Cummings J. H., Macfarlane G. T. Role of intestinal bacteria in nutrient metabolism. J. Parenter. Enteral. Nutr. 1997;21:357–365.  [PubMed] Custodio J. M., Wu C. Y., Benet L. Z. Predicting drug disposition, absorption/elimination/transporter interplay and the role of food on drug absorption. Adv. Drug Deliv. Rev. 2008;60:717–733.[PMC free article]  [PubMed] Dantzig A. H., Shepard R. L., Law K. L., Tabas L., Pratt S., Gillespie J. S., Binkley S. N., Kuhfeld M. T., Starling J. J., Wrighton S. A. Selectivity of the multidrug resistance modulator, LY335979, for P-glycoprotein and effect on cytochrome P-450 activities. J. Pharmacol. Exp. Ther. 1999;290:854–862.[PubMed] Davies E. Sweets for my sweet. Chem. World. 2010;7:46–49. Decherf S., Demeneix B. A. The obesogen hypothesis: A shift of focus from the periphery to the hypothalamus. J. Toxicol. Environ. Health B. 2011;14:423–448.  [PubMed] Deichmann W. B., MacDonald W. E., Cubit D. A., Beasley A. G. Effects of starvation in rats with elevated DDT and dieldrin tissue levels. Int. Arch. Arbeitsmed. 1972;29:233–252.  [PubMed] Dekant W., Assmann M., Urban G. The role of cytochrome P450 2E1 in the species-dependent biotransformation of 1,2-dichloro-1,1,2-trifluoroethane in rats and mice. Toxicol. Appl. Pharmacol. 1995;135:200–207.  [PubMed] de Ruyter J. C., Olthof M. R., Seidell J. C., Katan M. B. A trial of sugar-free or sugar-sweetened beverages and body weight in children. N. Engl. J Med. 2012;367:1397–1406.  [PubMed] Desta Z., Soukhova N., Mahal S. K., Flockhart D. A. Interaction of cisapride with the human cytochrome P450 system: Metabolism and inhibition studies. Drug Metab. Dispos. 2000;28:789–800.  [PubMed] Desta Z., Wu C. M., Morocho A. M., Flockhart D. A. The gastroprokinetic and antiemetic drug metoclopramide is a substrate and inhibitor of cytochrome P450 2D6. Drug Metab. Dispos. 2002;30:336–343.  [PubMed] Dhingra R., Sullivan L., Jacques P. F., Wang T. J., Fox C. S., Meigs J. B., D'Agostino R. B., Gaziano J. M., Vasan R. S. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007;116:480–488.[

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