A study entitled “Fructose intervention for 12 weeks does not impair glycemic control for incretin hormone responses during oral glucose or mixed meal tests in obese men” by Matikainen et al. was recently published in Nutrition, Metabolism & Cardiovascular Diseases. The purpose of the study was to determine if habitual fructose consumption (75g/d for 12 weeks) resulted in incretin mediated worsening of glycemic control.

Researchers recruited “healthy obese men” based on the following criteria: waist circumference ˃ 96cm, body mass index (BMI) between 27 and 40 kg/m², stable weight for the last 3 months, low-density lipoprotein cholesterol (LDL-C) < 4.5 mmol/l and triglycerides (TG) < 5.5 mmol/l. None of the subjects reported taking any medications or hormones known to mediate glucose of lipoprotein metabolism. A total of 65 participants completed the study with full data sets.

Each subject consumed their normal diet supplemented with 75g of fructose daily for 12 weeks. Fructose was provided in lemon flavored carbonated beverages prepared as 7.6% (w/w). Participants received three, 330ml bottles per day equaling 303 kcals from the fructose sweetened beverages. They were instructed to consume their beverages together with their three main meals while maintaining their normal ad libitum diets and physical activity routines. Each participant kept a 3-day food record before the intervention and then again within 2 weeks of the conclusion of the intervention.

Prior to the start of the fructose intervention, subjects participated in 3 study visits: 1) oral glucose tolerance test (OGTT), 2) mixed meal test, 3) magnetic resonance imaging. During the mixed meal test, participants were asked to consume a meal (63g Carbohydrate, 56g Fat, 40g Protein, 927kcals) followed by a series of blood draws. Magnetic resonance spectroscopy was used to measure liver fat content.

Researchers note the following results:

• On average, participants were 48 years old and had a BMI of 30.6 kg/m² (obese)
• Before the intervention, there were no correlations between fasting GLP-1 or GIP with BMI, liver fat, subcutaneous fat, visceral fat, fasting glucose, or fasting insulin.
• Fasting GLP-1 was correlated with HOMA-IR prior to intervention.
• During the OGTT – glucose, insulin, GLP-1 and GIP responses were similar before and after the fructose intervention.
• Fasting HOMA-IR, insulinogenic index, and disposition index did not change significantly during the fructose intervention.
• Fasting and postprandial PYY concentrations were not affected by fructose intervention.
• Fructose intervention did increase fasting TG slightly by significantly (mean: 1.56 (before) 1.66 (after) p-value 0.032).
• Post prandial TG was also higher after fructose intervention.
• GLP-1 and GIP did not differ before or after fructose intervention during the mixed meal test.
• The fructose intervention resulted in an increased energy intake but this was not statistically significant.
• The 12 week fructose intervention resulted in a slight but significant increase in weight from 99.2kg to 100kg.
• Liver fat increased 9.2% but subcutaneous and visceral fat did not change.
• After dividing data up by weight stable, weight gain, and weight loss groups and conducting statistical analysis, researchers found that the result remained the same.
• After dividing data up by liver fat responses, they found that the liver fat increase group had higher TG, fasting insulin, and HOMA-IR.

Researchers conclude “that 75 g daily fructose from SSBs for 12 weeks does not impair gut incretin response or glucose tolerance in obese males, even in the presence of moderate weight- or liver fat gain.”

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N. Matikainen 1 S. Söderlund 1 E. Björnson C.F. Deacon J. Borén 2 M.-R. Taskinen 2. Fructose intervention for 12 weeks does not impair glycemic control or incretin hormone responses during oral glucose or mixed meal tests in obese men. Matikainen et al. March 18, 2017. DOI:https://doi.org/10.1016/j.numecd.2017.03.003

On April 18, Caliceti et al. published a review entitled “Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review” in Nutrients. The review focuses on the role of uric acid (UA) in cardio metabolic disorders and the relationship between fructose consumption, blood UA, and health outcomes.

The authors first review purine metabolism including purine generation via two pathways 1) purine salvage pathway and 2) de novo synthesis from non-purine compounds followed the catabolism of purines which is regulated by xanthine-oxidoreductase (XOR) which codes for the xanthine dehydrogenase (XDH) and xanthine oxidase (XO) enzymes. The mechanisms of XDH and XO result in UA production. Authors note that most UA is filtered through the kidneys and is excreted in the urine, the rest is metabolized by gut microbiota in the intestine and is eliminated in the feces. UA reabsorption and secretion have a number of mediators that help regulate UA concentrations.

Authors note that metabolism of fructose is known to stimulate UA production through purine degradation which generates mitochondrial oxidants. The mitochondrial oxidative stress results in stimulation of fatty acid synthase and therefore promotes de novo lipogenesis and hepatic fat accumulation. Authors also cite researcher suggesting that fructose stimulates UA synthesis from amino acid precursors such as glycine and that chronic fructose consumption can inhibit renal excretion of UA resulting increased serum UA, though this last point is not well supported.

Next, author’s present data which suggest that UA can act as an intracellular prooxidant under inflammatory conditions, as in the case of arterial plaque formation. UA has also been found to induce intracellular oxidative stress by stimulating NOX and altering mitochondrial function which can result in fat synthesis. Another oxidative stress hypothesis is that intracellular XO activity and increased reactive oxygen species (ROS) production can result in endothelial dysfunction and lead to hypertension.

Authors then detail in vivo literature pertaining to the topic which is largely contradictory and controversial due to the inability for population-based studies to adjust for confounding variables. The paper concludes “a specific causal link between fructose consumption, hyperuricemia, and CVS has not yet been established…it is not yet possible to conclude that fructose intake is the main contributor to an increase in blood UA, and that this detrimentally affects vascular health.”

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