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The cardiovascular disease (CVD) risk of metabolically healthy obesity (MHO) remains controversial. We sought to further characterize the CVD risk profile in MHO by evaluating postprandial triglycerides, vascular function, and systemic inflammatory markers. Control individuals that were normal-weight and metabolically healthy (Con), MHO, and metabolic syndrome (MetS) were recruited (n = 10–11/group). Each participant underwent an abbreviated fat tolerance test, fasting and postprandial flow-mediated dilation (FMD), and had a panel of inflammatory cytokines measured. MHO displayed postprandial triglycerides similar to those in Con and both MHO and Con had lower values than those for MetS (p < 0.01). Fasting FMD was lower in MHO and MetS compared to that of Con (p < 0.01), but during the postprandial period the vasodilatory response of MHO was similar to that while fasting (p = 0.39), while FMD in Con and MetS decreased after the high-fat meal (p values < 0.01). MHO displayed a number of inflammatory cytokines greater than those of Con and MetS (all p values < 0.05), while MetS and MHO had higher TNF-α than did Con (p < 0.05). In conclusion, MHO was associated with lower fasting FMD and a greater inflammatory burden but did not suffer the same negative postprandial effects as did MetS.

Introduction: Normal-weight obesity (NWO) is defined as having a normal BMI yet high body fat % and is linked to increased cardiovascular disease (CVD) risk. However, the current understanding of NWO’s risk profile is incomplete and, in many cases, their clinical presentation is arguably unremarkable based on common risk factors. Hypothesis: We hypothesized that other indictors of CVD risk such as postprandial triglycerides (TG), flow-mediated dilation (FMD), and inflammatory cytokines would be elevated in NWO, consistent with their future CVD risk. Methods: Individuals were recruited into 3 groups (n = 10/ group): healthy controls (Con), NWO, and metabolic syndrome (MetS) based on results from a fasting metabolic panel, blood pressure, and DEXA. All participants underwent an abbreviated fat tolerance test where fasting TG were measured, a high-fat shake was consumed (9 kcal/kg; 73% fat), and then TG measured again 4 hrs later. Brachial FMD was measured during the fasted state and postprandially, and a high-sensitivity T cell cytokine bioplex (Millipore; Burlington, MA) was performed with fasting serum. Data were analyzed using one-way ANOVA followed by Fisher’s LSD. Results: NWO and MetS had similar body fat % and both were higher than Con ( p < 0.01). All groups differed with respect to visceral adipose tissue mass, with MetS > NWO > Con ( p < 0.01). Despite having similar fasting TG to Con, NWO (122.5 ± 46.4 mg/dL) had 4-hr TG intermediate to Con (73.7 ± 13.9 mg/dL) and MetS (178.3 ± 76.4 mg/dL; p < 0.01). Across the entire sample, FMD decreased ( p < 0.01) after the high-fat meal. MetS (3.3 ± 1.2 %) displayed lower fasting FMD than Con (5.1 ± 1.1 %), and NWO (4.5 ± 2.0 %) was similar to both groups ( p < 0.05). No group differences were observed with postprandial FMD. The majority of cytokines assessed were not different across groups. However, MetS (7.8 ± 2.1 pg/mL) exhibited higher TNF-α than Con (4.8 ± 1.9 pg/mL; p < 0.05), and NWO (6.6 ± 3.4 pg/mL) was not different from either group. Conclusions: In conclusion, NWO was associated with higher postprandial TG than Con, but displayed little evidence of impaired vascular health or inflammation. MetS had the greatest 4-hr TG, as well as impaired vascular function and signs of inflammation compared to Con.

Post-meal triglycerides are an independent cardiovascular disease (CVD) risk factor, but the ideal high-fat meal formulation has yet to be standardized and is one challenge prohibiting widespread clinical adoption of postprandial triglyceride assessment. Two general approaches often used are giving individuals a high-fat meal scaled to body weight or a standardized high-fat meal containing a set fat bolus. A recent expert panel statement has endorsed the latter, specifying 75 g of fat as an appropriate fat dosage. Despite this recommendation, no study to date has tested whether there is a difference in postprandial triglycerides or if risk classification is affected based on these different approaches. We recruited 16 generally healthy individuals with roughly equal distribution among body mass index (BMI)class (n = 5–6/per BMI category) and sex (n = 2–3 M/F) within each BMI class. Each participant underwent two abbreviated fat tolerance tests separated by ~1 week: one with a scaled to body weight high-fat meal (9 kcal/kg; 70% fat) and a standardized meal containing 75 g of fat (70% fat). Fasting, 4 h, and absolute change in triglycerides across the entire sample and within each BMI category were similar regardless of high-fat meal. Only one participant with obesity had discordant postprandial responses between the fat tolerance tests (i.e., different CVD risk classification). These findings suggest that, within a certain range of fat intake, generally healthy individuals will have a similar postprandial triglyceride response. Considering the greater convenience of utilizing standardized high-fat meals, our data suggest that a standardized high-fat meal may be acceptable for large-scale studies and clinical implementation.

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