Gaining fat during late adolescence may worsen insulin resistance
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Key takeaways:
- Young people who have increases in fat mass at age 17 and 24 years have higher odds for elevated insulin resistance.
- Higher fat mass also raises the likelihood for hyperglycemia and hyperinsulinemia.
Adolescents who have an increase in fat mass are more likely to have worse insulin resistance as young adults, according to study findings published in The Journal of Clinical Endocrinology & Metabolism.
“Interrupting fat mass increase in late adolescence before the fat mass-insulin resistance vicious cycle at age 17 through 24 years begins will likely prevent the onset of type 2 diabetes in later life,” Andrew O. Agbaje, MD, MPH, clinical researcher in the Institute of Public Health and Clinical Nutrition, School of Medicine at University of Eastern Finland, and honorary research fellow at the Children’s Health and Exercise Research Center in the department of public health and sports sciences at the University of Exeter in the U.K., told Healio. “Health care providers should consider excess total fat and abdominal fat at age 17 years as an emergency that should be urgently addressed.”
Agbaje and colleagues collected data from 3,160 adolescents participating in the Avon Longitudinal Study of Parents and Children birth cohort who had full body composition and metabolic outcome data available. Total body fat mass, trunk fat mass and total body lean mass were measured through a DXA scan at age 15, 17 and 24 years. Fasting blood samples were collected at all three follow-ups. Participants were considered at risk for hyperglycemia if they had a fasting glucose of more than 6.1 mmol/L and at risk for hyperinsulinemia with an insulin level of more than 11.78 mU/L. Homeostasis model of insulin resistance and the single-point insulin sensitivity estimator were calculated for each participant.
Both males and females had an increase in fat mass and lean mass from age 15 years to age 24 years. Fasting glucose, insulin and insulin resistance decreased from age 15 years to age 17 years before increasing from age 17 years to age 24 years.
After adjusting for covariates, each 1 kg increase in total fat mass and trunk fat mass, and each 1 kg/m2 increase in BMI from age 15 to age 24 years increased the likelihood for hyperglycemia, hyperinsulinemia and elevated insulin resistance (P < .001 for all). Each 1 kg increase in lean mass lowered the risk for hyperinsulinemia (P = .007) and elevated insulin resistance (P = .009). Cumulative increases in total fat mass, trunk fat mass, BMI and lean mass were all inversely associated with single-point insulin sensitivity estimator score.
“Each 1 kg increase in trunk fat raises the risk of progressively worsening insulin resistance by 21% while total body fat increases the risk by 12%,” Agbaje said. “This suggests that abdominal fat may be twice as dangerous as body fat in potentially causing insulin resistance. However, increasing muscle mass may slightly reduce the risk of insulin resistance.”
Cumulative HDL and LDL cholesterol, triglycerides, systolic blood pressure and lean mass partially mediated the association between increased fat mass and increased insulin resistance. LDL cholesterol had a 41% mediation effect on the association between increased lean mass and decreased insulin resistance. Cumulative increased fat mass had an 85% mediation on the longitudinal associations between increased lean mass and increased insulin resistance.
“We have [previously] shown that at least 3 to 4 hours per day of light physical activity may significantly lower fat mass and reverse the adverse effect of sedentariness, while engaging in moderate to vigorous physical activity may increase muscle mass,” Agbaje said. “Combining these two physical activity intensities may be critical to non-pharmacologically preventing the fat mass-insulin resistance vicious cycle. Nonetheless, intervention studies, especially randomized clinical trials, are needed to confirm these findings in the young population.”
For more information:
Andrew O. Agbaje, MD, MPH, can be reached at andrew.agbaje@uef.fi.
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