Why the study?
Individuals with metabolically healthy obesity and normal-weight obesity often have clinically unremarkable risk profiles despite increased cardiovascular disease risk, prompting examination of less-utilized cardiometabolic risk factors in these groups.
Does an abbreviated fat tolerance test and measurement of FMD and inflammatory cytokines reveal increased cardiovascular risk in individuals with metabolically healthy obesity or normal-weight obesity?
Does an abbreviated fat tolerance test and measurement of FMD and inflammatory cytokines reveal increased cardiovascular risk in individuals with metabolically healthy obesity or normal-weight obesity?
Individuals with metabolically healthy obesity and normal-weight obesity exhibit subclinical cardiometabolic abnormalities, such as impaired FMD, low-grade inflammation, and exaggerated postprandial lipemia, suggesting increased cardiovascular risk despite unremarkable standard risk profiles.
Objectives: Individuals with metabolically healthy obesity (MHO) and normal-weight obesity (NWO) often present with clinically unremarkable risk profiles despite evidence of increased cardiovascular disease (CVD) risk. We therefore examined whether other, less-utilized cardiometabolic risk factors may be abnormal in these populations, consistent with their potential CVD risk. Methods: Two studies were conducted (N=41) measuring postprandial triglycerides after an abbreviated fat tolerance test (9 kcal/kg; 70% fat), the indicator of vascular health flow-mediated dilation (FMD) both pre- and post-high-fat meal, and a panel of fasting inflammatory cytokines. Study 1 evaluated these measures in MHO (body mass index [BMI] > 30 kg/m²; 0-1 metabolic syndrome [MetS] components) compared to metabolically healthy, normal-weight controls (BMI 18.5-24.9 kg/²2; 0-1 MetS components) and individuals with obesity and MetS (BMI > 30 kg/m²; 2+ MetS components). Study 2 examined the same parameters in NWO (BMI 18.5-24.9 kg/m²; body fat percent > 25% [M] or > 35% [F]) versus low body fat percent, normal-weight controls (BMI 18.5-24.9 kg/m²; body fat percent < 25% [M] or < 35% [F]; 0-1 MetS components) and those with obesity, high body fat percent, and metabolic syndrome (> 30 kg/m² body fat percent > 25% [M] or > 35% [F]; 2+ MetS components). Results: In study 1, MHO displayed similar postprandial triglycerides to normal-weight, metabolically healthy controls, and both groups were lower than MetS (p < 0.01). MHO and MetS both presented with lower fasting FMD than controls, but MHO did not experience the same decrease in FMD following the high-fat meal as other study groups (p = 0.39). Relative to controls, and in some cases MetS, MHO displayed consistent evidence of low-grade inflammation (e.g., higher interleukin [IL]-1β, IL-6; p’s < 0.05). In study 2, NWO participants had similar fasting triglycerides to normal-weight, lower body fat controls, but all groups differed with respect to postprandial triglycerides such that MetS > NWO > controls (p < 0.05). Conversely, NWO had similar flow-mediated dilation metrics and inflammatory mediators compared to low body fat counterparts. Conclusion: Overall, both MHO and NWO displayed evidence of increased CVD risk when these nontraditional risk factors were considered.
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Bryant Henry Keirns (2023) studied this question.
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