No difference in fat oxidation, postexercise energy expenditure or energy intake following ingestion of a protein-based breakfast compared to carbohydrate breakfast.

Background: Manipulation of macronutrient intake and exercise can alter overall energy consumption and potentially body composition. Aim: The purpose of this study was to manipulate the macronutrient content of breakfast before exercise to investigate the impact on exercise energy expenditure and postexercise energy intake (EI). Methods: Twelve active men were recruited, 11 finished the study protocol (age: 28 ± 9 years; VO2max: 56 ± 5 ml·kg-1·min-1). In a randomized crossover design, each participant completed 4 trials, 3 consisting of a specific breakfast (protein, PRO; carbohydrate, CHO; noncaloric; NON-CAL) followed in 1 h by a 45 minutes moderate intensity treadmill exercise protocol. The fourth trial consisted of breakfast and no exercise (CON). An ad-libitum lunch and food for the rest of the day were provided and assessed for EI. Measures included resting metabolic rate pre- and postbreakfast along with oxygen uptake (VO2) during and after exercise, along with hunger scales, and blood measures of glucose, insulin and plasma-PYY prebreakfast, pre-exercise, postexercise, and 60 minutes postexercise. Results: Fat oxidation was highest during exercise in the NON-CAL (0.57 g·min-1) trial with similar levels of fat oxidation between PRO (0.50 g·min-1) and CHO trials (0.48 g·min-1). Hunger was not affected by PRO intake or exercise, nor was appetite hormones and glucose. EI at lunch and dinner was not significantly different between trials. Conclusion: Pre-exercise PRO intake did not modify fat oxidation during exercise, did not lead to a larger VO2 versus CHO, nor did it attenuate EI postexercise.

Weight status and health behaviors of adolescents and young adults with sickle cell disease: The emerging risk for obesity.

Historically, youth with sickle cell disease (SCD) were at risk for being underweight, but recent data suggests this population is replicating obesity trends of youth in the United States. The current observational study assessed the weight status and health behaviors of 44 adolescents and young adults with SCD via a self-report survey and chart review. Using height and weight data closest to survey completion date, 27% of participants were either overweight or obese. With respect to obesogenic risk behaviors, 77% ate fast food 1-3 times per week, 25% had no fruits/vegetables with any of their meals, 11% drank no water, and 57% watched 4 or more hours of television per day. Though more research is needed, this preliminary study adds to the SCD literature suggesting an emerging shift toward obesity in this population. As such, adolescents with SCD may benefit from interventions to decrease obesity risk factors as being overweight or obese has the potential to worsen SCD-related symptoms and complications.

Body Composition Changes over Multiple Academic Years in Female Collegiate Soccer Players.

Body composition plays a key role in overall health and sports performance and its assessment is an important part of many athletic programs. The purpose of this study was to describe longitudinal changes in body composition for collegiate female soccer players in order to provide data to inform future training and nutrition interventions for this population. A linear mixed-model (LMM) approach was used to analyze four years of pre- and post-season body composition data, including total mass, fat-free mass (FFM), fat mass, and body fat percentage (%BF) for 49 athletes. Athletes gained an average of 0.5 kg FFM during the season (p < 0.05) and increased total mass, FFM, fat mass, and %BF (2.5 kg, 1.1 kg, 1.7 kg, and 1.7%, respectively; p < 0.05) over four years. Freshmen experienced a 1.5 kg gain in total mass pre- to post-season (p < 0.05), while no changes in total mass or body composition were seen in other grade levels. Gains in %BF during the off season between Freshman and Sophomore years represented negative changes in body composition that should be addressed further. These results can help interdisciplinary athlete care teams optimize training programs in this population by understanding what changes are expected over multiple years. Normalizing these changes may also help the promotion of realistic body composition goals and the development of positive training and dietary habits.

Evaluating a dietary pattern in adolescents with type 1 diabetes mellitus: The dash-d approach.

OBJECTIVE: Adolescents with type 1 diabetes (T1DM) must consider multiple factors in diet planning, including glycemic control and cardiovascular disease prevention, while ensuring adequate nutrition for growth. We examined diet composition, quality, and compliance for two dietary patterns - the traditional Dietary Approaches to Stop Hypertension (DASH) and a modified version of DASH in this population. METHODS AND FINDINGS: Two feeding studies were conducted. First, adolescents with T1DM consumed their usual diet for 3 days followed by traditional DASH for 6 days. Next, DASH menus were adjusted to align with T1DM nutrition guidelines, and this modified DASH for Diabetes (DASH-D) was tested on a new group of adolescents with T1DM for 6 days, following 3 days of usual diet. Usual diet was measured via 24-hr dietary recalls. Dietary composition of DASH-D was compared to DASH and usual diet. Eighteen adolescents (9/group) participated. Compared to usual diet, intake of protein, fiber, fruit, vegetables, lean meats, and low-fat dairy were higher, while saturated fat and added sugar were lower, in DASH-D. Percent energy from fat was higher, and from carbohydrate lower, in DASH-D versus traditional DASH, with food group intake reflecting these patterns. Participants consumed 87% of foods provided for DASH, and 98% of foods provided for DASH-D. In both DASH iterations, participants met national guidelines for fat, saturated fat, fiber, and fruit/vegetable intake, while usual diet fell short of these recommendations. CONCLUSIONS: The novel DASH-D pattern meets guidelines and may be a viable option for achieving nutrition goals for adolescents with T1DM.

PAR2 (Protease-Activated Receptor 2) Deficiency Attenuates Atherosclerosis in Mice.

OBJECTIVE: PAR2 (protease-activated receptor 2)-dependent signaling results in augmented inflammation and has been implicated in the pathogenesis of several autoimmune conditions. The objective of this study was to determine the effect of PAR2 deficiency on the development of atherosclerosis. APPROACH AND RESULTS: PAR2 mRNA and protein expression is increased in human carotid artery and mouse aortic arch atheroma versus control carotid and aortic arch arteries, respectively. To determine the effect of PAR2 deficiency on atherosclerosis, male and female low-density lipoprotein receptor-deficient (Ldlr-/-) mice (8-12 weeks old) that were Par2+/+ or Par2-/- were fed a fat- and cholesterol-enriched diet for 12 or 24 weeks. PAR2 deficiency attenuated atherosclerosis in the aortic sinus and aortic root after 12 and 24 weeks. PAR2 deficiency did not alter total plasma cholesterol concentrations or lipoprotein distributions. Bone marrow transplantation showed that PAR2 on nonhematopoietic cells contributed to atherosclerosis. PAR2 deficiency significantly attenuated levels of the chemokines Ccl2 and Cxcl1 in the circulation and macrophage content in atherosclerotic lesions. Mechanistic studies using isolated primary vascular smooth muscle cells showed that PAR2 deficiency is associated with reduced Ccl2 and Cxcl1 mRNA expression and protein release into the supernatant resulting in less monocyte migration. CONCLUSIONS: Our results indicate that PAR2 deficiency is associated with attenuation of atherosclerosis and may reduce lesion progression by blunting Ccl2- and Cxcl1-induced monocyte infiltration.

Associations between long chain polyunsaturated fatty acids and cardiovascular lipid risk factors in youth with type 1 diabetes: SEARCH Nutrition Ancillary Study.

PURPOSE: In this longitudinal study we explored the relationships between plasma n-3 and n-6 polyunsaturated fatty acids (PUFAs) and Δ5 and Δ6 desaturase activities (D5D and D6D, respectively) and fasting lipids in youth with type 1 diabetes (T1D). METHODS: Incident cases of T1D in youth <20years of age who were seen for a baseline study visit (N=914) and a 1-year follow-up visit (N=416) were included. Fasting blood samples were obtained at each visit and plasma phospholipid n-6 PUFAs were measured, which included linoleic acid (LA), dihomo-γ-linolenic acid (DGLA) and arachidonic acid (AA); n-3 PUFAs included α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Estimated D5D and D6D were calculated as FA product-to-precursor ratios, where D5D=AA/DGLA and D6D=DGLA/LA. To examine the longitudinal relationships between long chain PUFAs, desaturase activities and fasting plasma lipids in youth with T1D mixed effects models were used for each individual PUFAs, D5D and D6D, adjusted for demographics, clinic site, diabetes duration, insulin regimen, insulin dose/kg, HbA1c, insulin sensitivity score, and body mass index with random effects to account for the repeated measurements. FINDINGS: Favorable lipid associations were found between LA and low-density lipoprotein (LDL) cholesterol (ß=-0.58, p<0.05); AA, plasma triglycerides (TG) (ß=-0.04, p<0.05) and TG/high-density lipoprotein (HDL)-C ratio (ß=-0.04, p<0.05); and D5D, plasma TG (ß=-0.2, p<0.05) and TG/HDL-cholesterol ratio (ß=-0.23, p<0.05). Findings were mixed for the n-3 PUFAs and DGLA: ALA was positively associated with plasma TG (ß=0.33, p<0.05) and HDL cholesterol (ß=9.86, p<0.05); EPA was positively associated with total cholesterol (ß=8.17, p<0.05), LDL cholesterol (ß=5.74, p<0.01) and HDL cholesterol (ß=2.27, p<0.01); and DGLA was positively associated with TG/HDL-cholesterol ratio (ß=0.05, P<0.05). CONCLUSION: Findings suggest that the most abundant PUFA, LA as well as its metabolic bi-product AA, may be important targets for CVD lipid risk factor reduction in youth with T1D.

Effects of the dietary approaches to stop hypertension (DASH) diet on glucose variability in youth with Type 1 diabetes.

Objective: Glucose variability (GV) independently increases risk for vascular events in patients with diabetes. The Dietary Approaches to Stop Hypertension (DASH) dietary pattern emphasizes fruits, vegetables, whole grains, lean meats, and low fat dairy and has the potential to reduce postprandial blood glucose (BG) excursions, however, its effect on GV is not known. The purpose of this work was to assess feasibility and collect preliminary data on the efficacy of the DASH diet on GV in adolescents with type 1 diabetes (T1D). Methods: Twenty one adolescents recruited from the Diabetes Center of Cincinnati Children's Hospital Medical Center with T1D (11-17y) participated in one of two phases of a controlled feeding study. The first phase tested the acceptability and blood glucose response to a traditional DASH diet (DASH) and the second phase tested a DASH diet specifically modified for diabetes (DASH-D) to improve glucose response to meals. For each phase, participants consumed first their usual diet, and then a controlled DASH diet while wearing continuous glucose monitoring (CGM) systems for 3 days of each diet. All foods were provided to the patients during the DASH dietary periods and 24 h dietary recalls were conducted during the usual diet periods to assess daily intake. Results: Sixteen participants (14.1 +/- 2.2y) were included in final analyses (DASH n=7, DASH-D n=9). Both DASH diets were significantly higher in fruits, vegetables, fiber, vitamin A, and % energy from protein than usual intakes. DASH was higher in carbohydrate (CHO) (60 vs. 50%) and lower in fat (21 vs. 36%) than usual intake, resulting in higher GV (Standard Deviation and Lability Index) and more low BG excursions (3 ± 2.8 vs. 7.1 ± 3.3, p=0.024). DASH-D was modified to better match CHO and fat content of patients' usual intakes in phase 1 (50/30/20 for CHO/fat/pro respectively, which resulted in no difference in GV between DASH-D and usual intake. There were also trends for lower average BG (144.1 vs. 168.9, p=0.072) and less percentage of time spent in the hyperglycemic range (39.3 ± 25.5 vs. 54.1 ± 19.4, p=0.07) on DASH-D compared to usual intake. Conclusion: The DASH dietary pattern tended to result in less hyperglycemia and an overall lower BG compared to usual care. Modifying a traditional DASH diet by increasing heart healthy fats improves glycemic response to DASH and may be beneficial for long term cardiovascular benefits in youth with T1D.

Red Blood Cell Dysfunction Induced by High-Fat Diet: Potential Implications for Obesity-Related Atherosclerosis.

BACKGROUND: High-fat diet (HFD) promotes endothelial dysfunction and proinflammatory monocyte activation, which contribute to atherosclerosis in obesity. We investigated whether HFD also induces the dysfunction of red blood cells (RBCs), which serve as a reservoir for chemokines via binding to Duffy antigen receptor for chemokines (DARC). METHODS AND RESULTS: A 60% HFD for 12 weeks, which produced only minor changes in lipid profile in C57/BL6 mice, markedly augmented the levels of monocyte chemoattractant protein-1 bound to RBCs, which in turn stimulated macrophage migration through an endothelial monolayer. Levels of RBC-bound KC were also increased by HFD. These effects of HFD were abolished in DARC(-/-) mice. In RBCs from HFD-fed wild-type and DARC(-/-) mice, levels of membrane cholesterol and phosphatidylserine externalization were increased, fostering RBC-macrophage inflammatory interactions and promoting macrophage phagocytosis in vitro. When labeled ex vivo and injected into wild-type mice, RBCs from HFD-fed mice exhibited ≈3-fold increase in splenic uptake. Finally, RBCs from HFD-fed mice induced increased macrophage adhesion to the endothelium when they were incubated with isolated aortic segments, indicating endothelial activation. CONCLUSIONS: RBC dysfunction, analogous to endothelial dysfunction, occurs early during diet-induced obesity and may serve as a mediator of atherosclerosis. These findings may have implications for the pathogenesis of atherosclerosis in obesity, a worldwide epidemic.

Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults.

BACKGROUND: Studies show that obese individuals have prolonged elevations in postprandial lipemia and an exacerbated inflammatory response to high fat meals, which can increase risk for cardiovascular diseases. As epidemiological studies indicate an association between type of fat and circulating inflammatory markers, the purpose of this study was to investigate the acute effect of different fat sources on inflammation and oxidative stress in overweight and obese individuals. METHODS: Eleven overweight and obese subjects consumed three high fat milkshakes rich in monounsaturated fat (MFA), saturated fat (SFA), or long-chain omega 3 polyunsaturated fat (O3FA) in random order. Blood samples collected at baseline, 1, 2, 4, and 6 hours postprandial were analyzed for markers of inflammation (soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tumor necrosis factor- α (TNF-α), and C-reactive protein (CRP)), oxidative stress (8-epi-prostaglandin-F2α (8-epi) and nuclear factor-κB (NF-κB)), and metabolic factors (glucose, insulin, non-esterified free fatty acids, and triglycerides (TG)). RESULTS: O3FA enhanced NF-kB activation compared to SFA, but did not increase any inflammatory factors measured. Conversely, SFA led to higher ICAM-1 levels than MFA (p = 0.051), while MFA increased TG more than SFA (p < 0.05). CRP increased while TNF-α and 8-epi decreased with no difference between treatments. CONCLUSIONS: While most of the inflammatory factors measured had modest or no change following the meal, ICAM-1 and NF-κB responded differently by meal type. These results are provocative and suggest that type of fat in meals may differentially influence postprandial inflammation and endothelial activation.

Epigallocatechin-3-gallate (EGCG) attenuates inflammation in MRL/lpr mouse mesangial cells.

Epigallocatechin-3-gallate (EGCG), a bioactive component of green tea, has been reported to exert anti-inflammatory effects on immune cells. EGCG is also shown to activate the metabolic regulator, adenosine 5'-monophosphate-activated protein kinase (AMPK). Reports have also indicated that EGCG inhibits the immune-stimulated phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. The PI3K/Akt/mTOR pathway has been implicated in mesangial cell activation in lupus. Mesangial cells from MRL/lpr lupus-like mice are hyper-responsive to immune stimulation and overproduce nitric oxide (NO) and other inflammatory mediators when stimulated. In our current studies, we sought to determine the mechanism by which EGCG attenuates immune-induced expression of pro-inflammatory mediators. Cultured mesangial cells from MRL/lpr mice were pre-treated with various concentrations of EGCG and stimulated with lipopolysaccharide (LPS)/interferon (IFN)-gamma. EGCG activated AMPK and blocked LPS/IFN-gamma-induced inflammatory mediator production (iNOS expression, supernatant NO and interleukin-6). Interestingly, EGCG attenuated inflammation during AMPK inhibition indicating that the anti-inflammatory effect of EGCG may be partially independent of AMPK activation. Furthermore, we found that EGCG effectively inhibited the immune-stimulated PI3K/Akt/mTOR pathway independently of AMPK, by decreasing phosphorylation of Akt, suggesting an alternate mechanism for EGCG-mediated anti-inflammatory action in mesangial cells. Taken together, these studies show that EGCG attenuated inflammation in MRL/lpr mouse mesangial cells via the PI3K/Akt/mTOR pathway. Our findings suggest a potential therapeutic role for the use of EGCG to regulate inflammation and control autoimmune disease.

Inflammatory response to a high-fat, low-carbohydrate weight loss diet: effect of antioxidants.

The objective of this study was to test the hypothesis that the inflammatory response to a high-fat, low-carbohydrate weight loss diet (HF) we previously observed was due to oxidative stress. Nineteen overweight subjects (BMI>27 kg/m(2)) were randomly assigned to either an antioxidant supplement (AS) (1 g vitamin C/800 IU vitamin E) or a placebo (P) group and provided with a HF for 7 days. Fasted pre- and post serum samples were measured for markers of inflammation (C-reactive protein (CRP), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1)), oxygen radical absorbance capacity (ORAC), and glucose, whereas urine was measured for oxidative stress (8-epi-prostaglandin-F(2alpha) (8-epi)). HF resulted in significant reductions in weight (-3.2%), glucose (-18.7%), and MCP-1 (-15%) (all P<0.01), with no difference between groups. There was a trend for a differential effect between groups for CRP as it decreased 32% in the AS group but increased 50% for P (P=0.076). Inverse correlations were noted between initial values and changes in several inflammatory and oxidative stress markers, including CRP (r= -0.501), 8-epi (r= -0.863), and ORAC (r= -0.546) (all P<0.05). It was concluded that weight loss on a short-term HF caused reduction of some but not all markers of inflammation. A role for oxidative stress in causing inflammation was not confirmed; however, longer term diet-controlled studies are necessary to further explore the trend for a differential response in CRP with antioxidant supplementation.