Effect of Dietary Sugar Intake on Biomarkers of Subclinical Inflammation: A Systematic Review and Meta-Analysis of Intervention Studies

Abstract

It has been postulated that dietary sugar consumption contributes to increased inflammatory processes in humans, and that this may be specific to fructose (alone, in sucrose or in high-fructose corn syrup (HFCS)). Therefore, we conducted a meta-analysis and systematic literature review to evaluate the relevance of fructose, sucrose, HFCS, and glucose consumption for systemic levels of biomarkers of subclinical inflammation. MEDLINE, EMBASE, and Cochrane libraries were searched for controlled intervention studies that report the effects of dietary sugar intake on (hs)CRP, IL-6, IL-18, IL-1RA, TNF-α, MCP-1, sICAM-1, sE-selectin, or adiponectin. Included studies were conducted on adults or adolescents with ≥20 participants and ≥2 weeks duration. Thirteen studies investigating 1141 participants were included in the meta-analysis. Sufficient studies (≥3) to pool were only available for (hs)CRP. Using a random effects model, pooled effects of the interventions (investigated as mean difference (MD)) revealed no differences in (hs)CRP between fructose intervention and glucose control groups (MD: −0.03 mg/L (95% CI: −0.52, 0.46), I2 = 44%). Similarly, no differences were observed between HFCS and sucrose interventions (MD: 0.21 mg/L (−0.11, 0.53), I2 = 0%). The quality of evidence was evaluated using Nutrigrade, and was rated low for these two comparisons. The limited evidence available to date does not support the hypothesis that dietary fructose, as found alone or in HFCS, contributes more to subclinical inflammation than other dietary sugars.

Lactobacillus helveticus and Lactobacillus plantarum modulate renal antioxidant status in a rat model of fructose-induced metabolic syndrome

“…Overconsumption of fructose has been proposed as a risk factor for the metabolic syndrome, manifesting in dysfunctional adipose, liver, kidney, intestine and cardiovascular tissues [25]. One of the leading driving forces for the fructose-induced disturbances is the oxidative stress arising from an imbalance between the prooxidant and antioxidant systems [26]. This study demonstrated some favorable influences of probiotic supplementation with L. helveticus and L. plantarum on the metabolic parameters and renal antioxidant/ oxidant status of rats maintained on a high-fructose diet.…”

Adipose Tissue and Brain Metabolic Responses to Western Diet—Is There a Similarity between the Two?

“…Since increased intake of fat and fructose is associated with systemic and tissue inflammation [14,15], we wanted to verify whether this response was elicited after our dietary treatment. To this end, we assessed markers of inflammation in plasma, e-WAT and brain areas.…”

A proof of concept gene‐activated titanium surface for oral implantology applications

“…Because this coating is intended for use in the oral environment, limiting the total amount of sucrose available to saccharolytic oral bacteria is an important consideration. Although sucrose alone has not been found to induce inflammation in gingival tissue, growth of saccharolytic bacteria on titanium surfaces has been shown to be enhanced by repeated exposure to high‐concentration sucrose solutions, and the resulting biofilms can have inflammatory effects on local tissue (Della Corte et al, ; Hert, Fisk, Rhee, & Brunt, ; Khan, Ansari, & Haqqi, ; Murakami, Mealey, Mariotti, & Chapple, ; Souza et al, ). The 1% sucrose solution was therefore selected for use in later experiments to improve the translatability of this coating by reducing total sucrose available to oral bacteria.…”