Daily watermelon consumption decreases plasma sVCAM-1 levels in overweight and obese postmenopausal women.

Postmenopausal status is associated with an increase in total and abdominal body fat as well as increased incidence of insulin resistance and cardiovascular disease. The purpose of this study was to determine if watermelon supplementation affects select systemic markers of atherosclerosis and measures of insulin resistance in overweight and obese postmenopausal women. We hypothesized that overweight and obese postmenopausal women consuming 100% watermelon puree daily for 6 weeks would have improved levels of select systemic markers connected with cardiovascular disease without changing markers of insulin resistance. To test this hypothesis, overweight and obese postmenopausal women were recruited to participate in this study. Participants were randomly assigned to either the control group (no intervention) or the watermelon puree group (WM) for 6 weeks. Plasma concentration of markers connected with atherosclerosis and glycemic control were measured pre- and poststudy. A significant 6% decrease in soluble vascular cell adhesion molecule-1 occurred pre- to poststudy in WM, P = .003. The pattern of change in fasting blood glucose (P = .633), insulin (P = .158), and homeostatic model assessment-estimated insulin resistance (P = .174) did not differ between groups. Pre- to poststudy increases were measured in the fasting plasma concentration of l-arginine (8%, P = .005), cis-lycopene (32%, P = .003), and trans-lycopene (42%, P = .003) in WM. We conclude that 6 weeks of watermelon supplementation improved soluble vascular cell adhesion molecule-1 levels, a marker connected to atherogenesis, independent of changes in body composition or glycemic control.

Prevalence and domains of disability within and outside Appalachian North Carolina: 2013-2016 Behavioral Risk Factor Surveillance System.

BACKGROUND: The health and social conditions of the Appalachian region generally are poorer than in the US overall, and this gap is widening, suggesting disability may be higher in Appalachia. OBJECTIVE: To describe the prevalence of disability overall and by domain in Appalachian and non-Appalachian regions in North Carolina (NC) and describe the characteristics of people with and without disability in each region. METHODS: We conducted a cross-sectional study using data from the NC Behavioral Risk Factor Surveillance System from 2013 to 2016 which assessed disability in five domains: vision, cognitive, mobility, self-care, and independent living. We calculated weighted proportions and age- and sex-adjusted prevalence using direct standardization to the 2010 Census. RESULTS: The prevalence of disability in Appalachian NC was significantly higher than in non-Appalachian NC after standardizing by age and sex (26.6% in Appalachia, 24.1% outside Appalachia, p < 0.001). In both regions, mobility disability was most common and self-care disability was least common. People within Appalachia more frequently reported disability in all domains compared to people outside Appalachia. CONCLUSIONS: More than one in four adults in Appalachian North Carolina experience disability in at least one domain and one in eight experiences disability in multiple domains. The high prevalence of disability should be considered when planning programs and services across the spectrum of public health. Understanding common disability domains present in populations can inform public health agencies and service providers and help them develop programs and messaging that meet the needs of residents in Appalachia and are accessible to people with disabilities.

Validity of Urine Specific Gravity When Compared With Plasma Osmolality as a Measure of Hydration Status in Male and Female NCAA Collegiate Athletes.

Sommerfield, LM, McAnulty, SR, McBride, JM, Zwetsloot, JJ, Austin, MD, Mehlhorn, JD, Calhoun, MC, Young, JO, Haines, TL, and Utter, AC. Validity of urine specific gravity when compared with plasma osmolality as a measure of hydration status in male and female NCAA collegiate athletes. J Strength Cond Res 30(8): 2219-2225, 2016-The purpose of this study was to evaluate the response of urine specific gravity (Usg) and urine osmolality (Uosm) when compared with plasma osmolality (Posm) from euhydration to 3% dehydration and then a 2-hour rehydration period in male and female collegiate athletes. Fifty-six National Collegiate Athletic Association (NCAA) wrestlers (mean ± SEM); height 1.75 ± 0.01 m, age 19.3 ± 0.2 years, and body mass (BM) 78.1 ± 1.8 kg and 26 NCAA women's soccer athletes; height 1.64 ± 0.01 m, age 19.8 ± 0.3 years, and BM 62.2 ± 1.2 kg were evaluated. Hydration status was obtained by measuring changes in Posm, Uosm, Usg, and BM. Male and female subjects dehydrated to achieve an average BM loss of 2.9 ± 0.09% and 1.9 ± 0.03%, respectively. Using the medical diagnostic decision model, the sensitivity of Usg was high in both the hydrated and dehydrated state for males (92%) and females (80%). However, the specificity of Usg was low in both the hydrated and dehydrated states for males (10 and 6%, respectively) and females (29 and 40%, respectively). No significant correlations were found between Usg and Posm during either the hydrated or dehydrated state for males or females. Based on these results, the use of Usg as a field measure of hydration status in male and female collegiate athletes should be used with caution. Considering that athletes deal with hydration status on a regular basis, the reported low specificity of Usg suggests that athletes could be incorrectly classified leading to the unnecessary loss of competition.

Insulin sensitivity is related to fat oxidation and protein kinase C activity in children with acute burn injury.

Impaired fatty acid oxidation occurs with type 2 diabetes and is associated with accumulations of intracellular lipids, which may increase diacylglycerol (DAG), stimulate protein kinase C activity, and inactivate insulin signaling. Glucose and fat metabolism are altered in burn patients, but have never been related to intracellular lipids or insulin signaling. Thirty children sustaining >40% total body surface area burns were studied acutely with glucose and palmitate tracer infusions and a hyper-insulinemic euglycemic clamp. Muscle triglyceride, DAG, fatty acyl CoA, and insulin signaling were measured. Liver and muscle triglyceride levels were measured with magnetic resonance spectroscopy. Muscle samples from healthy children were controls for DAG concentrations. Insulin sensitivity was reduced and correlated with whole body palmitate beta-oxidation (P = .004). Muscle insulin signaling was not stimulated by hyper-insulinemia. Tissue triglyceride concentrations and activated protein kinase C-beta were elevated, whereas the concentration of DAG was similar to the controls. Free fatty acid profiles of muscle triglyceride did not match DAG. Insulin resistance following burn injury is accompanied by decreased insulin signaling and increased protein kinase C-beta activation. The best metabolic predictor of insulin resistance in burned patients was palmitate oxidation.

PPAR-alpha agonism improves whole body and muscle mitochondrial fat oxidation, but does not alter intracellular fat concentrations in burn trauma children in a randomized controlled trial.

BACKGROUND: Insulin resistance is often associated with increased levels of intracellular triglycerides, diacylglycerol and decreased fat beta-oxidation. It was unknown if this relationship was present in patients with acute insulin resistance induced by trauma. METHODS: A double blind placebo controlled trial was conducted in 18 children with severe burn injury. Metabolic studies to assess whole body palmitate oxidation and insulin sensitivity, muscle biopsies for mitochondrial palmitate oxidation, diacylglycerol, fatty acyl Co-A and fatty acyl carnitine concentrations, and magnetic resonance spectroscopy for muscle and liver triglycerides were compared before and after two weeks of placebo or PPAR-alpha agonist treatment. RESULTS: Insulin sensitivity and basal whole body palmitate oxidation as measured with an isotope tracer increased significantly (P = 0.003 and P = 0.004, respectively) after PPAR-alpha agonist treatment compared to placebo. Mitochondrial palmitate oxidation rates in muscle samples increased significantly after PPAR-alpha treatment (P = 0.002). However, the concentrations of muscle triglyceride, diacylglycerol, fatty acyl CoA, fatty acyl carnitine, and liver triglycerides did not change with either treatment. PKC-theta activation during hyper-insulinemia decreased significantly following PPAR-alpha treatment. CONCLUSION: PPAR-alpha agonist treatment increases palmitate oxidation and decreases PKC activity along with reduced insulin sensitivity in acute trauma, However, a direct link between these responses cannot be attributed to alterations in intracellular lipid concentrations.

Insulin sensitivity and mitochondrial function are improved in children with burn injury during a randomized controlled trial of fenofibrate.

OBJECTIVE: To determine some of the mechanisms involved in insulin resistance immediately following burn trauma, and to determine the efficacy of PPAR-alpha agonism for alleviating insulin resistance in this population. SUMMARY BACKGROUND DATA: Hyperglycemia following trauma, especially burns, is well documented. However, the underlying insulin resistance is not well understood, and there are limited treatment options. METHODS: Twenty-one children 4 to 16 years of age with >40% total body surface area burns were enrolled in a double-blind, prospective, placebo-controlled randomized trial. Whole body and liver insulin sensitivity were assessed with a hyperinsulinemic-euglycemic clamp, and insulin signaling and mitochondrial function were measured in muscle biopsies taken before and after approximately 2 weeks of either placebo (PLA) or 5 mg/kg of PPAR-alpha agonist fenofibrate (FEN) treatment, within 3 weeks of injury. RESULTS: The change in average daily glucose concentrations was significant between groups after treatment (146 +/- 9 vs. 161 +/- 9 mg/dL PLA and 158 +/- 7 vs. 145 +/- 4 FEN; pretreatment vs. posttreatment; P = 0.004). Insulin-stimulated glucose uptake increased significantly in FEN (4.3 +/- 0.6 vs. 4.5 +/- 0.7 PLA and 5.2 +/- 0.5 vs. 7.6 +/- 0.6 mg/kg per minute FEN; pretreatment vs. posttreatment; P = 0.003). Insulin trended to suppress hepatic glucose release following fenofibrate treatment (P = 0.06). Maximal mitochondrial ATP production from pyruvate increased significantly after fenofibrate (P = 0.001) and was accompanied by maintained levels of cytochrome C oxidase and citrate synthase activity levels. Tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 in response to insulin increased significantly following fenofibrate treatment (P = 0.04 for both). CONCLUSIONS: Fenofibrate treatment started within 1 week postburn and continued for 2 weeks significantly decreased plasma glucose concentrations by improving insulin sensitivity, insulin signaling, and mitochondrial glucose oxidation. Fenofibrate may be a potential new therapeutic option for treating insulin resistance following severe burn injury.

Contraction of insulin-resistant muscle normalizes insulin action in association with increased mitochondrial activity and fatty acid catabolism.

Acute exercise can reverse muscle insulin resistance, but the mechanism(s) of action are unknown. With the use of a hindlimb perfusion model, we have found that acute contraction restores insulin-stimulated glucose uptake in muscle of obese Zucker rats to levels witnessed in lean controls. Previous reports have suggested that obesity-related insulin resistance stems from lipid oversupply and tissue accumulation of toxic lipid intermediates that impair insulin signaling. We reasoned that contraction might activate hydrolysis and oxidation of intramuscular lipids, thus alleviating "lipotoxicity" and priming the muscle for enhanced insulin action. Indeed, analysis of mitochondrial-derived acyl-carnitine esters suggested that contraction caused robust increases in beta-oxidative flux and mitochondrial oxidation. As predicted, contraction decreased intramuscular triacylglycerol content; however, diacylglycerol and long chain acyl-CoAs, lipid intermediates presumed to trigger insulin resistance, were either unchanged or increased. In muscles from obese animals, insulin-stimulated tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 remained impaired after contraction, whereas phosphorylation of the downstream signaling protein, AS160, was partially restored. These results suggest that acute exercise enables diabetic muscle to circumvent upstream defects in insulin signal transduction via mechanisms that are more tightly coupled to increased mitochondrial energy metabolism than the lowering of diacylglycerol and long chain acyl-CoA.