Objectives:Prenatal and early life factors such as Gestational Diabetes Mellitus (GDM), exclusive breastfeeding (EBF), and early exposure to sugar-sweetened beverages (SSBs) may contribute to obesity in children. The relationship of EBF and SSBs with obesity prevalence in children exposed to GDM has rarely been evaluated. This study examined the association of EBF and early SSBs consumption with obesity prevalence in children (1-5y) born to mothers with and without GDM.

Methods:This study used data from the 2014 Los Angeles County Women, Infants, and Children(WIC) Survey, which included 3,707 mothers and their children (1-5y). Infants (1-2y) with weight-for-height ≥ 97.7percentile were classified as subjects with high weight-for-length and children (2-5y) were classified as subjects with obesity if their BMI-for-age was ≥ 95percentile.

Results:The individual and combination interaction effects of GDM, SSBs intake, and EBF on obesity prevalence were all significant ( < 0.05). Compared to GDM offspring, with low SSBs intake, and who were EBF (referent), those who were GDM, with high SSBs intake and who were EBF had approximately a five-fold increase in odds of obesity (OR = 4.77, 95%CI 1.55-8.60, = 0.03). Compared to the GDM referent group, GDM offspring who were not EBF with low and high SSBs intake had 4.3- and 4.4-times higher odds of obesity, respectively (OR = 4.33, 95%CI 1.42- 8.07, = 0.01; OR = 4.38, 95%CI 1.39- 8.16, = 0.01). Using non-GDM, EBF and low SSBs as referent, those who were not EBF, with either high or low SSBs had approximately a 4-fold increase in odds of obesity (OR = 3.62, 95%CI: 2.16-6.05, < 0.0001; OR = 3.83, 95%CI: 2.26-6.48, < 0.0001).Compared to the non-GDM referent group, those who were EBF and had high SSBs intake had 77% higher odds of obesity (OR = 1.77, 95%CI 0.93-3.37, = 0.001).

Conclusions:In non-GDM offspring, EBF was protective against odds of obesity in both high and low SSBs consumers. In GDM offspring, EBF was only protective against obesity when SSBs intake was low. Surprisingly, GDM offspring who were EBF and had high SSBs consumption had a 4- to 5-fold increase in odds of obesity compared to those not EBF with either low or high SSBs intake. These results suggest that interventions should focus on the combined protective effects of EBF and low SSBs intake, particularly in GDM offspring.

Funding Sources:First 5 LA.

AIMS:Glucose effectiveness (GE) refers to the ability of glucose to influence its own metabolism through insulin-independent mechanisms. Diminished GE is a predictor of progression to type 2 diabetes. Exercise training improves GE, however, little is known about how dietary interventions, such as manipulating the glycemic index of diets, interact with exercise-induced improvements in GE in at-risk populations.

METHODS:We enrolled 33 adults with obesity and pre-diabetes (17 males, 65.7 ± 4.3 years, 34.9 ± 4.2 kg m) into a 12-week exercise training program (1 h dayand 5 day weekat ~ 85% of maximum heart rate) while being randomized to concurrently receive either a low (EX-LOG: 40 ± 0.3 au) or high (EX-HIG: 80 ± 0.6 au) glycemic index diet. A 75-g oral-glucose-tolerance test (OGTT) was performed before and after the intervention and GE was calculated using the Nagasakaequation. Insulin resistance was estimated using a hyperinsulinemic-euglycemic clamp and cardiorespiratory fitness using a VOtest.

RESULTS:Both EX-LOG and EX-HIG groups had similar improvements in weight (8.6 ± 5.1 kg, P < 0.001), VO(6 ± 3.5 mL kg min, P < 0.001) and clamp-measured peripheral insulin resistance (1.7 ± 0.9 mg kg min, P < 0.001), relative to baseline data. GE in EX-LOG and EX-HIG was similar at baseline (1.9 ± 0.38 vs. 1.85 ± 0.3 mg dL min, respectively; P > 0.05) and increased by ~ 20% post-intervention in the EX-LOG arm (∆GE: 0.07-0.57 mg dL min, P < 0.05). Plasma free fatty acid (FFA) concentrations also decreased only in the EX-LOG arm (∆FFA: 0.13 ± 0.23 mmol L, P < 0.05).

CONCLUSIONS:Our data suggest that a high glycemic index diet may suppress exercise-induced enhancement of GE, and this may be mediated through plasma FFAs.

Consumption of a high-fat, high-sugar diet and sedentary lifestyle are correlated with bulk arterial stiffening. While measurements of bulk arterial stiffening are used to assess cardiovascular health clinically, they cannot account for changes to the tissue occurring on the cellular scale. The compliance of the subendothelial matrix in the intima mediates vascular permeability, an initiating step in atherosclerosis. High-fat, high-sugar diet consumption and a sedentary lifestyle both cause micro-scale subendothelial matrix stiffening, but the impact of these factors in concert remains unknown. In this study, mice on a high-fat, high-sugar diet were treated with aerobic exercise or returned to a normal diet. We measured bulk arterial stiffness through pulse wave velocity and subendothelial matrix stiffness ex vivo through atomic force microscopy. Our data indicate that while diet reversal mitigates high-fat, high-sugar diet-induced macro- and micro-scale stiffening, exercise only significantly decreases micro-scale stiffness and not macro-scale stiffness, during the time-scale studied. These data underscore the need for both healthy diet and exercise to maintain vascular health. These data also indicate that exercise may serve as a key lifestyle modification to partially reverse the deleterious impacts of high-fat, high-sugar diet consumption, even while macro-scale stiffness indicators do not change.