Greater Fructose Consumption Is Associated with Cardiometabolic Risk Markers and Visceral Adiposity in Adolescents3

Abstract

Though adolescents consume more fructose than any other age group, the relationship between fructose consumption and markers of cardiometabolic risk has not been established in this population. We determined associations of total fructose intake (free fructose plus one-half the intake of free sucrose) with cardiometabolic risk factors and type of adiposity in 559 adolescents aged 14-18 y. Fasting blood samples were measured for glucose, insulin, lipids, adiponectin, and C-reactive protein. Diet was assessed with 4-7 24-h recalls and physical activity (PA) was determined by accelerometry. Fat-free soft tissue (FFST) mass and fat mass were measured by DXA. The s.c. abdominal adipose tissue (SAAT) and visceral adipose tissue (VAT) were assessed using MRI. Multiple linear regression, adjusting for age, sex, race, Tanner stage, FFST mass, fat mass, PA, energy intake, fiber intake, and socioeconomic status, revealed that fructose intake was associated with VAT (β = 0.13; P = 0.03) but not SAAT (P = 0.15). Significant linear upward trends across tertiles of fructose intake were observed for systolic blood pressure, fasting glucose, HOMA-IR, and C-reactive protein after adjusting for the same covariates (all P-trend < 0.04). Conversely, significant linear downward trends across tertiles of fructose intake were observed for plasma HDL-cholesterol and adiponectin (both P-trend < 0.03). When SAAT was added as a covariate, these trends persisted (all P-trend < 0.05). However, when VAT was included as a covariate, it attenuated these trends (all P-trend > 0.05). In adolescents, higher fructose consumption is associated with multiple markers of cardiometabolic risk, but it appears that these relationships are mediated by visceral obesity.

Diverse roles for theDrosophilafructose sensor Gr43a

“…In humans, the increase of fructose consumption is strongly associated with a steady increase in obesity, insulin resistance, and other metabolic syndromes. 44,45 In addition, several studies in humans and mice suggest that fructose and glucose, the most common dietary sugars, are absorbed in distinct regions of the gastrointestinal tract and metabolized differently, 46,47 and that fructose and glucose affect brain activity and feeding behavior in a disparate manner. 48,49 Thus, it will be interesting to see whether this sugar-and a specific receptor for it-plays also a role in nutrient sensing in mammals.…”

Letter by Malavazos et al Regarding Article, “Sweetened Beverage Consumption, Incident Coronary Heart Disease, and Biomarkers of Risk in Men”

“…The consequent lower activation of lipoprotein lipase in subcutaneous adipose tissue increases availability of triglycerides and their uptake into VAT. 3 This dietary fructose-visceral fat relationship has also been reported in a recent article by Pollock et al, 4 who conclude that greater fructose consumption is associated with multiple markers known to increase the risk for cardiovascular disease, such as blood lipids and inflammatory adipocytokines, suggesting that these relationships are dependent on visceral obesity.…”

Fructose Intake and Cardiovascular Risk Factors in Youth with Type 1 Diabetes: The SEARCH for Diabetes in Youth Study

“…Inadequate statistical power (n=16) and short follow-up period (1 week) may have limited the ability to detect group differences in this trial. In a larger, more recent crosssectional study of adolescents without T1D, total fructose consumption was found to be associated with increased plasma triglycerides and LDL-cholesterol and low HDLcholesterol (31). Among healthy Swiss children, dietary fructose was found to be a significant positive predictor of small LDL-particle size (a marker for increase CVD risk) but not plasma triglycerides (32).…”