SUMMARY Elephant seals are naturally adapted to survive up to three months of absolute food and water deprivation (fasting). Prolonged food deprivation in terrestrial mammals increases reactive oxygen species (ROS) production, oxidative damage and inflammation that can be induced by an increase in the renin–angiotensin system (RAS). To test the hypothesis that prolonged fasting in elephant seals is not associated with increased oxidative stress or inflammation, blood samples and muscle biopsies were collected from early (2–3 weeks post-weaning) and late (7–8 weeks post-weaning) fasted seals. Plasma levels of oxidative damage, inflammatory markers and plasma renin activity (PRA), along with muscle levels of lipid and protein oxidation, were compared between early and late fasting periods. Protein expression of angiotensin receptor 1 (AT₁), pro-oxidant (Nox4) and antioxidant enzymes (CuZn- and Mn-superoxide dismutases, glutathione peroxidase and catalase) was analyzed in muscle. Fasting induced a 2.5-fold increase in PRA, a 50% increase in AT₁, a twofold increase in Nox4 and a 70% increase in NADPH oxidase activity. By contrast, neither tissue nor systemic indices of oxidative damage or inflammation increased with fasting. Furthermore, muscle antioxidant enzymes increased 40–60% with fasting in parallel with an increase in muscle and red blood cell antioxidant enzyme activities. These data suggest that, despite the observed increases in RAS and Nox4, an increase in antioxidant enzymes appears to be sufficient to suppress systemic and tissue indices of oxidative damage and inflammation in seals that have fasted for a prolonged period. The present study highlights the importance of antioxidant capacity in mammals during chronic periods of stress to help avoid deleterious systemic consequences.

First-year college students are at particular risk of dietary maladaptation during their transition to adulthood. A college environment that facilitates consistent access to nutritious food is critical to ensuring dietary adequacy among students. The objective of the study was to examine perceptions of the campus food environment and its influence on the eating choices of first-year students attending a minority-serving university located in a food desert. Focus group interviews with twenty-one first-year students were conducted from November 2016 to January 2017. Students participated in 1 of 5 focus groups. Most interviewees identified as being of Hispanic/Latino or Asian/Pacific Islander origin. A grounded theory approach was applied for inductive identification of relevant concepts and deductive interpretation of patterns and relationships among themes. Themes related to the perceived food environment included adequacy (i.e., variety and quality), acceptability (i.e., familiarity and preferences), affordability, and accessibility (i.e., convenience and accommodation). Subjective norms and processes of decisional balance and agency were themes characterizing interpersonal and personal factors affecting students’ eating choices. The perceived environment appeared to closely interact with subjective norms to inform internal processes of decision-making and agency around the eating choices of first-year students attending a minority-serving university campus located in a food desert.

Activation of angiotensin receptor type 1 (AT1) contributes to NADPH oxidase (Nox)-derived oxidative stress during metabolic syndrome. However, the specific role of AT1 in modulating redox signaling, mitochondrial function, and oxidative stress in the heart remains more elusive. To test the hypothesis that AT1 activation increases oxidative stress while impairing redox signaling and mitochondrial function in the heart during diet-induced insulin resistance in obese animals, Otsuka Long Evans Tokushima Fatty (OLETF) rats ( n = 8/group) were treated with the AT1 blocker (ARB) olmesartan for 6 wk. Cardiac Nox2 protein expression increased 40% in OLETF compared with age-matched, lean, strain-control Long Evans Tokushima Otsuka (LETO) rats, while mRNA and protein expression of the H₂O₂-producing Nox4 increased 40–100%. ARB treatment prevented the increase in Nox2 without altering Nox4. ARB treatment also normalized the increased levels of protein and lipid oxidation (nitrotyrosine, 4-hydroxynonenal) and increased the redox-sensitive transcription factor Nrf2 by 30% and the activity of antioxidant enzymes (SOD, catalase, GPx) by 50–70%. Citrate synthase (CS) and succinate dehydrogenase (SDH) activities decreased 60–70%, whereas cardiac succinate levels decreased 35% in OLETF compared with LETO, suggesting that mitochondrial function in the heart is impaired during obesity-induced insulin resistance. ARB treatment normalized CS and SDH activities, as well as succinate levels, while increasing AMPK and normalizing Akt, suggesting that AT1 activation also impairs cellular metabolism in the diabetic heart. These data suggest that the cardiovascular complications associated with metabolic syndrome may result from AT1 receptor-mediated Nox2 activation leading to impaired redox signaling, mitochondrial activity, and dysregulation of cellular metabolism in the heart.

The transition to nutritional independence makes new college students vulnerable to alterations in eating patterns, which can increase the risk of cardiometabolic disorders. The aim of the study was to examine the potential benefits of almond vs. cracker snacking in improving glucoregulatory and cardiometabolic profiles in new college students. A randomized controlled, parallel-arm, 8-week intervention of 73 college students (BMI: 18–41 kg/m²) with no cardiometabolic disorders was conducted. Participants were randomized into either an almond snack group (56.7 g/day; 364 kcal; n = 38) or Graham cracker control group (77.5 g/day; 338 kcal/d; n = 35). Chronic, static changes were assessed from fasting serum/plasma samples at baseline, and after 4 and 8 weeks. Acute, dynamic effects were assessed during a 2-h oral glucose tolerance test (OGTT) at 8 weeks. Almond snacking resulted in a smaller decline in HDL cholesterol over 8 weeks (13.5% vs. 24.5%, p < 0.05), 13% lower 2-h glucose area under the curve (AUC), 34% lower insulin resistance index (IRI) and 82% higher Matsuda index (p < 0.05) during the OGTT, despite similar body mass gains over 8 weeks compared with the cracker group. In general, both almond and cracker snacking reduced fasting glucose, and LDL cholesterol. Conclusions: Incorporating a morning snack in the dietary regimen of predominantly breakfast-skipping, first-year college students had some beneficial effects on glucoregulatory and cardiometabolic health. Almond consumption has the potential to benefit postprandial glucoregulation in this cohort. These responses may be influenced by cardiometabolic risk factor status.

Renin-angiotensin system blockade improves glucose intolerance and insulin resistance, which contribute to the development of metabolic syndrome. However, the contribution of impaired insulin secretion to the pathogenesis of metabolic syndrome is not well defined. To assess the contributions of angiotensin receptor type 1 (AT₁) activation and high glucose intake on pancreatic function and their effects on insulin signaling in skeletal muscle and adipose tissue, an oral glucose tolerance test (oGTT) was performed in five groups (n = 10/group) of rats: 1) lean strain-control 2) obese Otsuka Long-Evans Tokushima Fatty (OLETF), 3) OLETF + angiotensin receptor blocker (ARB; 10 mg/kg · d olmesartan for 6 wk; OLETF ARB), 4) OLETF + 5% glucose water (HG) for 6 wk (OLETF HG), and 5) OLETF + HG + ARB (OLETF HG/ARB). The glucose response to the oGTT increased 58% in OLETF compared with lean-strain control, whereas glucose supplementation increased it an additional 26%. Blockade of angiotensin receptor reduced the oGTT response 19% in the ARB-treated groups and increased pancreatic insulin secretion 64 and 113% in OLETF ARB and OLETF HG/ARB, respectively. ARB treatment in OLETF ARB and OLETF HG/ARB did not have an effect on insulin signaling proteins in skeletal muscle; however, it reduced pancreatic AT₁ protein expression 20 and 27%, increased pancreatic glucagon-like peptide-1 (GLP-1) receptor protein expression 41 and 88%, respectively, and increased fasting plasma GLP-1 approximately 2.5-fold in OLETF ARB. The results suggest that improvement of glucose intolerance is independent of an improvement in muscle insulin signaling, but rather by improved glucose-stimulated insulin secretion associated with decreased pancreatic AT₁ activation and increased GLP-1 signaling.

Under normal conditions cardiac tissue utilizes roughly 70% fatty acids (FA), and 30% glucose to produce ATP; however, during impaired metabolic conditions like insulin resistance and diabetes, gluco...