Postprandial triglycerides across the aging spectrum: A secondary analysis utilizing an abbreviated fat tolerance test.

BACKGROUND & AIMS: Elevated postprandial triglycerides are an independent cardiovascular disease risk factor and observed in older adults. However, differences in postprandial triglycerides across the spectrum of adulthood remain unclear. METHODS AND RESULTS: We performed a secondary analysis of six studies where adults (aged 18-84 years; N = 155) completed an abbreviated fat tolerance test (9 kcal/kg; 70% fat). Differences in postprandial triglycerides were compared in those ≥50 and <50 years and by decade of life, adjusting for sex and BMI. Compared to those <50 years, participants ≥50 years had higher fasting, 4 h, and Δ triglycerides from baseline (p's < 0.05). When examining triglyceride parameters by decade, no differences were observed for fasting triglycerides, but 50 s, 60 s, and 70s-80 s displayed greater 4 h and Δ triglycerides versus 20 s (p's ≤ 0.001). The frequency of adverse postprandial triglyceride responses (i.e., ≥220 mg/dL) was higher in participants ≥50 versus <50 years (p < 0.01), and in 60 s compared to all other decades (p = 0.01). CONCLUSION: Older age was generally associated with higher postprandial triglycerides, with no divergence across the spectrum of older adulthood. In our sample, postprandial triglyceride differences in older and younger adults were driven by those >50 years relative to young adults in their 20 s. REGISTRATION: N/A (secondary analysis).

Cardiorespiratory fitness and submaximal exercise dynamics in normal-weight obesity and metabolically healthy obesity.

PURPOSE: Cardiorespiratory fitness (CRF) is critical for cardiovascular health. Normal-weight obesity (NWO) and metabolically healthy obesity (MHO) may be at increased risk for cardiovascular disease, but a comparison of CRF and submaximal exercise dynamics against rigorously defined low- and high-risk groups is lacking. METHODS: Four groups (N = 40; 10/group) based on body mass index (BMI), body fat %, and metabolic syndrome (MetS) risk factors were recruited: healthy controls (CON; BMI 18.5-24.9 kg/m2, body fat < 25% [M] or < 35% [F], 0-1 risk factors), NWO (BMI 18.5-24.9 kg/m2, body fat ≥ 25% [M] or ≥ 35% [F]), MHO (BMI > 30 kg/m2, body fat ≥ 25% [M] or ≥ 35% [F], 0-1 risk factors), or metabolically unhealthy obesity (MUO; BMI > 30 kg/m2, body fat ≥ 25% [M] or ≥ 35% [F], 2 + risk factors). All participants completed a V ˙ O2peak test on a cycle ergometer. RESULTS: V ˙ O2peak was similarly low in NWO (27.0 ± 4.8 mL/kg/min), MHO (25.4 ± 6.7 mL/kg/min) and MUO (24.6 ± 10.0 mL/kg/min) relative to CON (44.2 ± 11.0 mL/kg/min) when normalized to total body mass (p's < 0.01), and adjusting for fat mass or lean mass did not alter these results. This same differential V ˙ O2 pattern was apparent beginning at 25% of the exercise test (PGroup*Time < 0.01). CONCLUSIONS: NWO and MHO had similar peak and submaximal CRF to MUO, despite some favorable health traits. Our work adds clarity to the notion that excess adiposity hinders CRF across BMI categories. CLINICALTRIALS: gov registration: NCT05008952.

Childhood psychosocial stress is linked with impaired vascular endothelial function, lower SIRT1, and oxidative stress in young adulthood.

Adverse childhood experiences (ACEs) are psychosocial stressors that occur during sensitive developmental windows and are associated with increased lifetime cardiovascular disease (CVD) risk in a dose-dependent manner. Vascular endothelial dysfunction is a pathophysiological mechanism that promotes hypertension and CVD and may be a mechanism by which ACEs contribute to lifetime CVD risk. We examined whether exposure to ACEs is associated with reduced vascular endothelial function (VEF) in otherwise healthy, young adult women (20.7 ± 3 yr) with (ACE+) versus without (ACE-) ACEs, explored whether differences in circulating sirtuin 1 (SIRT1) or systemic oxidative stress could explain ACEs-related differences in VEF, and examined the ability of a pilot, 8-wk exercise intervention to augment VEF and SIRT1 or reduce oxidized LDL cholesterol (oxLDL) in ACE+ young adult women. Forty-two otherwise healthy young adults completed this study. Prior to the intervention, VEF (P = 0.002) and SIRT1 (P = 0.004) were lower in the ACE+ than ACE- group, but oxLDL concentrations were not different (P = 0.77). There were also significant relationships (P ≤ 0.04) among flow-mediated dilation (FMD), SIRT1, and oxLDL in the ACE+, but not ACE- group. Adjusting for circulating SIRT1 and oxLDL reduced the differences in FMD observed between groups (P = 0.10), but only SIRT1 was a significant adjuster of the means (P < 0.05). Finally, the exercise intervention employed was unable to enhance VEF or SIRT1 in the ACE+ exercise group. Our data suggest that ACEs likely increase susceptibility to hypertension and CVD by causing endothelial dysfunction, perhaps through a SIRT1 pathway-related mechanism.NEW & NOTEWORTHY Our study provides novel evidence that young adult women with moderate-to-severe adverse childhood experience (ACE) exposure present impaired endothelial function and lower circulating sirtuin 1 (SIRT1) concentrations than age-matched controls. However, an 8-wk exercise intervention was unable to augment endothelial function or SIRT1 concentrations in a subset of those with ACEs. Our data suggest that ACEs-related impairments in endothelial function may be secondary to decreased NO bioavailability via SIRT1 and/or oxidative stress-related mechanisms.

Fibroblast Growth Factor 19: Potential modulation of hepatic metabolism for the treatment of non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver disease that is becoming more prevalent in concert with obesity and poor lifestyle habits. Although NAFLD is treatable via lifestyle modification in early stages, more advanced liver pathologies (eg non-alcoholic steatohepatitis [NASH]) are harder to reverse. There is no Food and Drug Administration approved pharmacological treatment for NAFLD, and little research has been done to identify compounds that target key NAFLD mechanisms. Bile acids and bile acid receptors have been implicated in NAFLD pathogenesis and modulating bile acids and bile acid receptors has recently been targeted as a therapeutic treatment option for NAFLD. Fibroblast growth factor 19 (FGF19), a nutritionally regulated post-prandial hormone, is a chief regulator of bile acid metabolism and an important player in lipid and carbohydrate metabolism, including key mechanisms of NAFLD pathogenesis. In this review, we discuss recent findings related to FGF19-regulated processes involved in the pathogenesis of NAFLD. We summarize known and conjectural frameworks and limitations for the clinical application of FGF19-targeted therapies as they relate to NAFLD.

Exercise and intestinal permeability: another form of exercise-induced hormesis?

Regular aerobic exercise has numerous benefits on human physiology, arguably by serving as a hormetic stressor resulting in positive adaptations over time. It has long been known that aerobic exercise at a variety of intensities and durations induces intestinal permeability, which is a feature of many pathologies of the gastrointestinal tract and metabolic diseases. Given the health benefits of exercise, it seems unlikely that intestinal permeability induced by exercise outweighs the positive adaptations. In fact, a growing body of evidence suggests adoption of exercise regimens lasting weeks to months improves indicators of intestinal permeability. In this brief review, we summarize factors contributing to acute exercise-induced intestinal permeability and what is known about chronic exercise and the gut barrier. Additionally, we outline known and theoretical adaptations of the gut to chronic exercise that may explain emerging reports that exercise improves markers of gut integrity.

Postprandial Metabolism and Vascular Function: Impact of Aging and Physical Activity Level.

The consumption of a high-fat meal can induce postprandial lipemia and endothelial dysfunction. The authors assessed the impact of age and physical activity on metabolic and vascular outcomes following meal consumption in healthy adults. The authors recruited four groups: younger active (age 22.1 ± 1.4 years; n = 9), younger inactive (age 22.6 ± 3.7 years; n = 8), older active (age 68.4 ± 7.7 years; n = 8), and older inactive (age 67.7 ± 7.2 years; n = 7). The metabolic outcomes were measured at the baseline and hourly for 6 hr post high-fat meal consumption (12 kcal/kg; 63% fat). Flow-mediated dilation was measured at the baseline, 2 hr, and 4 hr postmeal. The total area under the curve for triglycerides was significantly lower in the more active groups, but did not differ based on age (younger active = 6.5 ± 1.4 mmol/L × 6 hr, younger inactive = 11.7 ± 4.8, older active = 6.8 ± 2.7, older inactive = 12.1 ± 1.7; p = .0004). After adjusting for artery diameter, flow-mediated dilation differed between groups at the baseline (younger active = 4.8 ± 1.6%, younger inactive = 2.5 ± 0.5, older active = 3.4 ± 0.9, older inactive = 2.2 ± 0.4; p < .001) and decreased significantly across groups 4 hr postmeal (mean difference = 0.82; 95% CI [0.02, 1.6]; p = .04). These findings highlight the beneficial effect of regular physical activity on postprandial lipemia, independent of age.

Discordance between gut-derived appetite hormones and energy intake in humans.

Gut-derived hormones affect appetite and are thought to play an important role in body weight regulation. Dietary macronutrient composition can influence gut-derived appetite hormone concentrations, thereby providing theoretical basis for why some diets might facilitate weight loss better than others. We investigated postprandial gut-derived appetite hormones in 20 inpatient adults after 2 weeks of eating either a low carbohydrate (LC) or a low fat (LF) diet followed by the alternate diet in random order. A LC meal resulted in significantly greater postprandial GLP-1, GIP, and PYY but lower ghrelin compared to an isocaloric LF meal (all p≤0.02). However, differences in gut-derived appetite hormones were incommensurate with subsequent ad libitum energy intake over the rest of the day, which was 551±103 kcal (p<0.0001) greater with the LC as compared to the LF diet. The effects of gut-derived appetite hormones on ad libitum energy intake can be dominated by other diet-related factors, at least in the short-term.

Diet order affects energy balance in randomized crossover feeding studies that vary in macronutrients but not ultra-processing.

BACKGROUND: Crossover studies can induce order effects, especially when they lack a wash-out period. OBJECTIVE: To explore diet order effects on energy balance and food intake between randomized diet order groups in two inpatient crossover studies originally designed to compare within-subject differences in ad libitum energy intake between either minimally processed low carbohydrate (LC) versus low fat (LF) diets or macronutrient-matched diets composed of mostly minimally processed food (MPF) or ultra-processed food (UPF). METHODS: Diet order group comparisons of changes in body weight, body composition, and differences in energy expenditure, and food intake were assessed over four weeks in 20 adults randomized to either the LC followed immediately by the LF diet (LC→LF) or the opposite order (LF→LC) as well as 20 adults randomized to either the MPF followed by UPF (MPF→UPF) diets or the opposite order (UPF→MPF). RESULTS: Subjects randomized to LC→LF lost 2.9 ± 1.1 kg more body weight (p < 0.001) and 1.5 ± 0.6 kg more body fat (p = 0.03) than the LF→LC group likely because the LC→LF group consumed 922 ± 304 kcal/d less than the LF→LC group (p = 0.0024). Reduced energy intake in LC→LF vs LF→LC was driven by the last two weeks (-1610 ± 306 kcal/d; p<0.00001) perhaps due to carryover effects of gut adaptations over the first two weeks arising from large differences in the mass of food (1295 ± 209 g/d; p<0.00001) and fiber intake (58 ± 5 g/d; p<0.00001). There were no diet order effects on ad libitum energy intake, body weight, or body composition change between UPF→MPF versus MPF→UPF groups. CONCLUSIONS: Diet order influences daily ad libitum energy intake, body weight change, and fat change within the context of a 4-week crossover inpatient diet study varying in macronutrients, but not varying in extent and purpose of processing. Funding sources: Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. Clinical Trial Registration: NCT03407053 and NCT03878108.

Postprandial triglycerides and fibroblast growth factor 19 as potential screening tools for paediatric non-alcoholic fatty liver disease.

BACKGROUND: Better screening tools for paediatric NAFLD are needed. We tested the hypothesis that the postprandial triglyceride (TG) and fibroblast growth factor 19 (FGF19) response to an abbreviated fat tolerance test (AFTT) could differentiate adolescents with NAFLD from peers with obesity and normal weight. METHODS: Fifteen controls with normal weight (NW), 13 controls with obesity (OB) and 9 patients with NAFLD completed an AFTT. Following an overnight fast, participants consumed a high-fat meal. TG and FGF19 were measured at baseline and 4 h post-meal. Liver steatosis and fibrosis were measured via Fibroscan. RESULTS: Fasting TG and FGF19 did not differ among groups; 4 h TG in the NAFLD and OB groups were greater (197 ± 69 mg/dL; 157 ± 72 mg/dL, respectively) than NW (105 ± 45 mg/dL; p < 0.05) and did not differ from one another. Within the entire cohort, 4 h TG were stratified by high and low steatosis. Adolescents with high steatosis had 98% greater 4 h TG than adolescents with low steatosis. 4 h FGF19, but not fasting FGF19, was higher in children with low steatosis compared with high steatosis (p < 0.05). Using area under the receiver operating curve (AUROC), the only biochemical outcome with diagnostic accuracy for NAFLD was 4 h TG (0.77 [95% CI: 0.60-0.94; p = 0.02]). CONCLUSIONS: The postprandial TG response is increased in adolescents with obesity with hepatic steatosis, with or without NAFLD. Our preliminary analysis demonstrates 4 h TG differentiate patients with NAFLD from those without, supporting a role for the AFTT as a screening tool for paediatric NAFLD.

Whole-body bone mineral density and markers of bone homeostasis in adults with normal-weight obesity.

Background: Normal-weight obesity (NWO) describes individuals with a normal body mass index (BMI), but high body fat percent. NWO are at-risk for cardiometabolic diseases, but little is known about their bone health. Methods: Adults (N = 24) were classified as NWO (n = 12; 5M/7F) or low body fat percent controls (Con; n = 12; 6M/6F). Body composition and whole-body bone mineral density (BMD) were assessed using DXA. A serum bioplex assay was performed to examine markers related to bone formation and resorption. Results: In addition to higher body fat percent and visceral fat, NWO had lower whole-body BMD relative to Con (p's < 0.05). Circulating leptin was higher in NWO than Con (p < 0.05). Two biomarkers generally associated with lower bone mass - sclerostin and parathyroid hormone - were higher in NWO compared to Con (p's < 0.05). Conclusion: In this preliminary study, adults with NWO displayed lower whole-body BMD alongside evidence of bone resorption. Impaired bone health may be another subclinical risk factor present in NWO.

Progressive exercise training improves cardiovascular psychophysiological outcomes in young adult women with a history of adverse childhood experiences.

Adverse childhood experiences (ACEs) are early-life psychosocial stressors that are associated with poorer mental health and increased cardiovascular disease (CVD) risk in a dose-dependent manner. We examined the feasibility of an 8-wk combined aerobic and resistance exercise training program to improve systolic (SBP) and diastolic blood pressure (DBP), serum endothelin-1 (ET-1), resilience, hope agency, and hope pathways in young women with ACEs. Forty-two healthy women (21 ± 3 yr) with ≥4 (ACE+; n = 28) or 0 ACEs (ACE-; n = 14) participated in this study. Women with ACEs were randomly assigned to an exercise (ACE+EXT; n = 14) or nonexercise control (ACE+CON; n = 14) group, whereas all ACE- participants were assigned to a nonexercise control (n = 14) group. Hope agency and DBP did not change in any group (P ≥ 0.43), but hope pathways improved only in ACE+EXT (means ± SE change; +1.6 ± 0.74 au, P = 0.032, Hedges' g = 0.53). ET-1 decreased in ACE+EXT only (-0.31 ± 0.15 pg/mL, P = 0.043, g = 0.46). Although the interactions for resilience and SBP did not reach significance (P = 0.05-0.06), forced post hoc analyses indicated that resilience improved (+4.9 ± 1.9 au, P = 0.012, g = 0.64) and SBP tended to improve (-4.0 ± 2.0 mmHg, P = 0.053, g = 0.51) in ACE+EXT only. There were significant associations between changes in hope pathways and SBP (ρ = -0.43, P = 0.023) and ET-1 (ρ = -0.53, P = 0.005), and between changes in SBP and ET-1 (ρ = 0.49; P = 0.012) in the ACE+ group. In summary, structured exercise training reduces serum ET-1 levels, improves positive psychological coping, and may improve SBP in young women with ACEs. The relationships among the changes in hope pathways, SBP, and ET-1 suggest a cardiovascular psychophysiological relationship in young women with ACEs.NEW & NOTEWORTHY This randomized controlled pilot trial shows, for the first time, that 8 wk of structured, progressive exercise training lowers serum endothelin-1 (ET-1) and improves positive psychological coping in young women with significant early-life psychosocial stress. Furthermore, the observed associations among changes in psychological attributes, ET-1, and systolic blood pressure signify a potential interplay between positive psychology and cardiovascular disease risk among women with adverse childhood experiences.

Adverse childhood experiences and obesity linked to indicators of gut permeability and inflammation in adult women.

Gut permeability may increase cardiovascular disease risk by allowing bacterial components (e.g., lipopolysaccharide or LPS) to enter the bloodstream, leading to low-grade inflammation. People with adverse childhood experiences (ACEs) consistently display evidence of chronic inflammation, but the source of this inflammation, and whether gut permeability may contribute, is unknown. Moreover, whether ACE status may further perturb obesity-associated gut permeability and inflammation is unknown. Women (N = 79, aged 18-84y) free of cardiometabolic diseases and inflammatory conditions and not regularly taking anti-inflammatory medications were included in a 2 × 2 factorial design with low or high ACE status (either 0 ACEs or 3+ ACEs) and body mass index (BMI) (either normal-weight [18.5-24.9 kg/m2; NW] or obesity [>30 kg/m2; OB]) as factors (n = 15-27/group). Serum LPS binding protein (LBP), soluble CD14 (sCD14), fatty-acid binding protein-2 (FABP2), LPS core IgM, and the ratio of LBP:sCD14 were used as indicators of gut permeability. Inflammatory markers C-reactive protein (CRP), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 were also measured. Data were analyzed using 2-way ANCOVA (age-adjusted). LBP, LBP:sCD14 and FABP2 were higher in OB versus NW, regardless of ACE status (PBMI < 0.05). Higher ACE status was associated with increased circulating LBP:sCD14 and LPS core IgM (PACE < 0.05). sCD14 was unrelated to BMI or ACEs. CRP was elevated in OB versus NW (PBMI < 0.001) and tended to be higher with 3+ ACEs compared to 0 ACEs (PACE = 0.06). Moreover, TNF-α was greater in 3+ ACEs relative to 0 ACEs (PACE = 0.03). IL-6 was unrelated to BMI or ACE status. No interaction effects were observed for any marker of gut permeability or inflammation. In sum, ACE status and obesity were independently associated with evidence of gut permeability and systemic inflammation but did not interact in relation to indicators of gut permeability.

Comparison of a Standardized High-Fat Meal versus a High-Fat Meal Scaled to Body Mass for Measuring Postprandial Triglycerides: A Randomized Crossover Study.

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.

Associations between Internalized Weight Stigma and Visceral Adipose Tissue Status are Observed in Women but not Men.

Purpose: This study investigated the relationship between internalized weight stigma (IWS) and visceral adipose tissue (VAT), an independent predictor of cardiometabolic disease risk, and how this relationship is moderated by gender. Methods: Participants (N=70, 81% white, 51% women, M age=30.4±7.8 years, M BMI=28.7±5.5 kg/m2, M BF%=32.4±8.9%) completed in-lab measures of demographic factors (age, gender, race/ethnicity), IWS (Weight Bias Internalization Scale-Modified; WBIS-M) and visceral adiposity. VAT mass was measured via DXA. Primary moderation analysis investigated the effect of gender on associations between IWS and VAT mass. Covariates were age, race/ethnicity, and total body fat percent. Results: After adjusting for covariates in the primary moderation analysis, WBIS-M scores displayed a positive association with VAT mass (b=32.58, p=0.033). The relationship between WBIS-M scores and VAT mass was moderated by gender (b=68.63, p=0.020); no relationship between WBIS-M scores and VAT mass was observed in men (b=-2.71, p=0.894), whereas a positive association between WBIS-M scores and VAT mass was observed in women (b=65.92, p=0.003). Conclusions: Internalization of weight stigma was associated with greater visceral adiposity in women across the BMI spectrum, suggesting it as a chronic stressor. Future studies should investigate directionality and causality of this relationship to elucidate mechanisms of stigma-associated CVD risk.

Postprandial triglycerides, endothelial function, and inflammatory cytokines as potential candidates for early risk detection in normal-weight obesity.

PROBLEM: Normal-weight obesity (NWO) is associated with increased cardiovascular disease (CVD) risk. However, NWO's clinical presentation is often unremarkable based on common risk factors. We examined whether CVD risk factors not routinely measured clinically including postprandial triglycerides, flow-mediated dilation (FMD), and inflammatory cytokines would be abnormal in NWO, consistent with their future risk. METHODS: Individuals were recruited into 3 groups (n = 10/ group): controls (Con), NWO, and metabolic syndrome (MetS). Con was defined as a normal body mass index (BMI), < 25% (M) or < 35% (F) body fat, and < 1 International Diabetes Federation (IDF) criteria. NWO were above this body fat cutoff while maintaining a normal BMI and MetS was defined per the IDF. Participants underwent an abbreviated fat tolerance test (i.e., difference in fasting and 4 h triglycerides following a high-fat meal [9 kcal/kg; 73% fat)] and fasting and postprandial lipid and glucose metrics, as well as FMD were measured. A T cell cytokine bioplex was also performed using fasting serum. RESULTS: NWO and MetS had similar body fat% and both were higher than Con (p < 0.0001). Despite having similar fasting triglycerides to Con, NWO had 4-hour triglycerides 66% greater than Con, but 46% lower than MetS (p < 0.01). FMD decreased in all groups after the high-fat meal (p < 0.0001). MetS displayed lower fasting FMD than Con, and NWO was similar to both groups (p < 0.05). No group differences were observed with postprandial FMD and the majority of fasting cytokines assessed. However, MetS exhibited higher fasting TNF-α than Con (p < 0.05), and NWO was similar to both groups. CONCLUSIONS: Overall, NWO was associated with higher postprandial triglycerides than Con, but displayed little evidence of impaired vascular health or inflammation.

The effect of black coffee on fasting metabolic markers and an abbreviated fat tolerance test.

BACKGROUND & AIMS: Coffee is typically prohibited prior to metabolic assessment in clinical and research settings. However, whether coffee meaningfully alters fasted metabolic testing or the results of a fat tolerance test is unclear. We investigated whether allowing black coffee intake within a fast prior to blood work affected fasting triglycerides (TG) and glucose, as well as the postprandial lipemic and glycemic response following an abbreviated fat tolerance test (AFTT). METHODS: Participants completed two randomized AFTTs separated by at least 1 week. For each AFTT, participants arrived into the laboratory following a 10 h overnight fast and consumed either 8 oz of water or black coffee. Thirty minutes later, a baseline blood draw was collected. Immediately following, participants consumed a standardized high-fat shake (70% fat; 9 kcal/kg body mass), vacated the laboratory, and returned 4 h later for a follow-up blood draw. RESULTS: Ten healthy individuals (5M, 5F; age: 22.9 ± 3.8 years; BMI: 24.3 ± 2.6 kg/m2) completed the study. There was no difference between trials with regard to baseline TG (MD = 1.7 mg/dL; p = 0.74), 4 h TG (MD = 2.7 mg/dL; p = 0.75), Δ TG (MD = 4.4 mg/dL; p = 0.52), or % change TG (MD = 7.7%; p = 0.99). Similarly, following coffee consumption, baseline glucose was unchanged relative to water (MD = 0.4 mg/dL; p = 0.84) and there were no differences in postprandial glucose measures, including 4 h (MD = 0.9 mg/dL; p = 0.58), Δ (MD = 1.3 mg/dL; p = 0.31), and % change in glucose (MD = 1.6%; p = 0.29). CONCLUSION: In our small study sample, coffee intake prior to an AFTT did not affect baseline or postprandial TG and glucose. Therefore, coffee intake prior to an AFTT may not affect its validity.

The reliability of an abbreviated fat tolerance test: A comparison to the oral glucose tolerance test.

BACKGROUND & AIMS: Postprandial lipemia (PPL) is predictive of cardiovascular disease risk, but the current method for assessing PPL is a burdensome process. Recently, the validity of an abbreviated fat tolerance test (AFTT) has been demonstrated. As a continuation of this research, the purpose of this study was to determine the reliability of the AFTT and compare it to the reliability of the oral glucose tolerance test (OGTT). METHODS: In this randomized crossover trial, 20 healthy adults (10 male and 10 female) completed 2 AFTTs and 2 OGTTs, each separated by a 1-week washout. For the AFTT, triglycerides (TG) were measured at baseline and 4 h post-consumption of a high-fat meal, during which time participants were able to leave the lab. For the OGTT, we measured blood glucose at baseline and 2 h post-consumption of a 75-g pure glucose solution, and participants remained in the lab. To determine reliability, we calculated within-subject coefficient of variation (WCV) and intraclass correlation coefficient (ICC). RESULTS: The mean 4-h TG WCV for the AFTT was 12.6%, while the mean 2-h glucose WCV for the OGTT was 10.5%. ICC values for 4-h TG and TG change were 0.79 and 0.71, respectively, while ICC values for 2-h glucose and glucose change were 0.66 and 0.56, respectively. CONCLUSIONS: Based on WCV and ICC, the TG response to an AFTT was similarly reliable to the glucose response to an OGTT in our sample of healthy adults, supporting the AFTT's potential as a standard clinical test for determining PPL. However, reliability of the AFTT needs to be further tested in individuals at greater risk for cardiometabolic disease.

Who would benefit most from postprandial lipid screening?

BACKGROUND & AIMS: Individuals with fasting triglycerides (TG) <150 mg/dL can experience a deleterious postprandial TG response ≥220 mg/dL to a high-fat meal (HFM). The purpose of this study was to identify individuals based on fasting TG that would benefit most from additional postprandial screening. METHODS: We conducted a secondary analysis of 7 studies from our laboratories featuring 156 disease-free participants (64 M, 92 F; age 18-70 years; BMI 18.5-30 kg/m2). Participants observed a 10-12 h overnight fast, after which they consumed an HFM (10-13 kcal/kg body mass; 61-64% kcal from fat). Two methods were used to identify lower and upper fasting TG cut points. Method 1 identified the lower limit as the TG concentration at which ≥90% of individuals presented peak postprandial TG (PPTG) <220 mg/dL and the upper limit as the concentration which ≥90% of individuals presented PPTG ≥220 mg/dL. Method 2 utilized receiver operating characteristic (ROC) curves and identified the lower limit as the fasting TG concentration where sensitivity was ≈95% and the upper limit as the concentration at which specificity was ≈95%. RESULTS: In Method 1, 90% of individuals with fasting TG >130 mg/dL (>1.50 mmol/L) exhibited PPTG ≥220 mg/dL (≥2.50 mmol/L), while 100% of individuals with fasting TG <66 mg/dL (0.75 mmol/L) had PPTG that did not exceed 220 mg/dL (2.50 mmol/L). In Method 2, when sensitivity was ≈95%, the corresponding fasting TG concentration was 70 mg/dL (0.79 mmol/L). When specificity was ≈95%, the corresponding fasting TG concentration was 114 mg/dL (1.29 mmol/L). Based on methods 1 and 2, there was a moderate positive association (r = 0.37, p < 0.004) between fasting and PPTG for individuals with fasting TG between 70 and 130 mg/dL (0.79-1.50 mmol/L), in which 24% exhibited PPTG ≥220 mg/dL (≥2.50 mmol/L) while 76% did not. CONCLUSIONS: Postprandial TG testing is likely most useful for individuals with fasting TG concentrations between 70 and 130 mg/dL (0.79-1.50 mmol/L). Outside of this range, postprandial TG responses are largely predictable. Establishing a specific patient group for which postprandial TG testing is most useful may lead to earlier risk detection in these individuals.

Resistance exercise attenuates postprandial metabolic responses to a high-fat meal similarly in younger and older men.

This study examined whether an acute bout of resistance exercise (RE) attenuated postprandial responses to a high fat meal (HFM) similarly in younger versus older adult men, and probed relationships among skeletal muscle mass (SMM), age, the metabolic load index (MLI) response, and the improvement in the MLI elicited by RE versus CON. Eleven younger (24 ±â€¯4y) and 9 older (61 ±â€¯5y) men completed RE or control (CON) the night prior to a HFM. Before and 1, 3, and 5 hours after the HFM, blood triglycerides (TG), glucose (GLU), MLI, and cholesterol concentrations were quantified. Following a 7 ±â€¯1-day washout period, participants returned and completed the opposite condition. Independent of age, TGs were 32.1 ±â€¯27.1 mg/dL and 52.7 ±â€¯26.8 mg/dL lower in RE than CON at 3 and 5 hours, respectively. MLI was also 24.3 to 56.9 mg/dL lower in RE than CON from 1 to 5 hours post-meal independent of age. The TG and MLI area under the curves (AUCs) were 15% to 31% lower in RE than CON. The GLU response was greater in the older than younger men at 1 to 5 hours post-meal. Moreover, the average GLU response was 5.6 ±â€¯2.5 mg/dL lower in RE versus CON and was inversely related to SMM across the sample (r = -0.615). However, age, volume, or SMM were not related to the MLIAUC, nor to the improvement elicited by RE. Therefore, although the older men displayed a greater postprandial glucose response than the younger men, RE attenuated the postprandial metabolic response to a HFM similarly in younger and older men.