Resistance training can alter a number of health-related and performance variables. These alterations include beneficial effects on body composition, blood pressure, and blood lipids and enhanced maximum strength, rate of force development, and power. These enhancements may translate into a better quality of life. As a result, resistance training can be used as a valuable tool in ameliorating the effects of a sedentary lifestyle, including those associated with metabolic syndrome. Nineteen subjects (10 metabolic syndrome, 9 previously sedentary nonmetabolic syndrome) underwent 8 weeks of supervised resistance training. After training, strength and V̇O2 peak increased by approximately 10% in the metabolic and nonmetabolic syndrome groups and the male and female groups. Percent body fat decreased in subjects with the metabolic syndrome and in females. Additionally, lean body mass increased in all groups (p<0.05). Eight weeks of resistance training improves several cardiovascular risk factors of metabolic syndrome.

BACKGROUND: Microvascular dysfunction (MD: impaired performance of blood flow, tissue perfusion, blood pressure, etc.) is one of the earliest stages in the progression of various chronic diseases. OBJECTIVE: The aim of this study was to determine if a difference in microvascular function existed between two metabolically healthy groups that differed in BMI and waist circumference. DESIGN: This study employed a causal comparative design, with two groups: I) normal weight (n =14, BMI 28 kg/m2). METHODS: Microvascular function was assessed by measuring skin blood flow (SkBF) using laser Doppler flowmetry during postocclusive reactive hyperemia (PORH). The area under the SkBF time curve during the 60-second PORH response was used to quantify the magnitude of the microvascular response. RESULTS: Group I (control) had a significantly higher average area under the SkBF time curve (3240 ± 879) than Group II (1948 ± 808) (Z= -3.0094, p = 0.0026). CONCLUSIONS: The overweight/obese subjects exhibited a diminished skin blood flow response to occlusion compared to their normal-weight counterparts. This supports the hypothesis that overweight/obese subjects who are otherwise metabolically healthy exhibit a biological change that is linked to chronic disease.

Prediabetes is defined by elevated blood glucose concentrations not high enough to meet criteria for type 2 diabetes. Exercise or metformin, a common “anti-diabetes” medication, may attenuate the progression from prediabetes to type 2 diabetes by improving insulin sensitivity and cardio-metabolic health. Because each treatment has its primary action in different tissues, combining exercise (muscle) with metformin (liver) may further enhance insulin sensitivity and cardio-metabolic health. Purpose: To determine the efficacy of combining exercise training with metformin on insulin sensitivity and cardio-metabolic health in men and women with prediabetes. We hypothesized that the combined treatment would improve insulin sensitivity and cardio-metabolic health more than either treatment alone. Methods: Thirty-two men and women with prediabetes were placed in placebo (P), metformin (M), exercise training and placebo (EP), or exercise training and metformin (EM) groups. Pill distribution was double-blind, and the groups were well-matched for age, weight, and fitness. There were no baseline differences in any characteristic. Subjects were provided P or 2000mg/d of M for 12 weeks and EM and EP underwent a progressive training protocol. Insulin sensitivity was measured 28-30hr post-exercise with a euglycemic hyperinsulinemic clamp. Traditional cardio-metabolic measures were also collected in the fasted state (e.g. blood pressure, blood lipids and inflammation). Group means were compared using a 2-way repeated measures analysis of variance. Results: Relative to baseline, all 3 interventions increased insulin sensitivity (p < 0.05), however, EP increased insulin sensitivity approximately 25-30% more than either EM or M. Compared to control, EP and M both lowered systolic blood pressure and C-reactive protein (p < 0.05, p = 0.06) and these reductions were approximately 15% more than EM. Each treatment raised HDL (p < 0.05). Enhanced insulin sensitivity was associated with increased non-oxidative glucose metabolism (i.e. glucose storage) (r = 0.85; p < 0.01). Conclusions: Despite more weight loss (4 kg), metformin blunted, rather than accentuated the effects of training on enhancing insulin sensitivity and lowering systolic blood pressure and inflammation. Given that metformin and physical activity are widely recommended treatments for prediabetes, it is important to better understand the mechanisms and ramifications of the combined treatment.

Osteoarthritis (OA) is a common and incapacitating joint disease beginning with breakdown of articular cartilage and extending into subchondral bone. At present, the processes through which the disease occurs are poorly understood, and interventions are limited to pain relief and eventual joint replacement. OA is commonly associated with obesity and corresponding pathologies, and as OA is demonstrably not a product of passive erosion of cartilage over time or under increased loads there must needs be some other mechanistic link between the two conditions. We hypothesize that the production of ceramides, a hallmark of the insulin resistance syndrome underlying many obesity-related conditions, acts to induce OA through its pro-inflammatory and pro-apoptotic activities, as well as directly inhibiting intracellular mediators of cartilage production and homeostasis. We demonstrate in Wistar rats that a high-fat, high-sugar (HFHS) diet successfully induces OA and that downregulation of ceramide synthesis through intraperitoneal myriocin administration does not prevent this degradation, and that myriocin in conjunction with a standard chow diet actually induces OA. Alteration in OA biomarkers in this study are discussed. We then tested the efficacy of a topical regimen of wogonin, an anti-inflammatory, anti-oxidative, and potentially analgesic compound in a surgical destabilization model (DMM) of OA in mice and demonstrate its disease modifying anti-OA properties. We further test the efficacy of this compound on the HFHS model previously established and find it successfully ameliorated the morphology and biomarker changes associated with OA; based on this data we hypothesize that inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is the most relevant physiological target of wogonin in a HFHS-induced OA model. Lastly and separately, we seek to clarify conflicting data regarding secondhand smoke (SHS), which observational studies suggest having either deleterious or beneficial effects to preexisting OA. In the first controlled study on the subject we model we demonstrate in a murine DMM model that SHS accelerates cartilage degradation and patterns of biomarker expression characteristic of OA, eliminating the question of any potential benefits of SHS to articular cartilage.

Bone-derived osteocalcin has been suggested to be a metabolic regulator. To scrutinize the relation between osteocalcin and peripheral insulin sensitivity, we analyzed changes in serum osteocalcin relative to changes in insulin sensitivity, low-grade inflammation, and bone mineral density following lifestyle-induced weight loss in individuals with metabolic syndrome (MetS). Participants with MetS were randomized to a weight loss program or to a control group. Before and after the 6-month intervention period, clinical and laboratory parameters and serum osteocalcin levels were determined. Changes in body composition were analyzed by dual-energy X-ray absorptiometry (DXA). In participants of the intervention group, weight loss resulted in improved insulin sensitivity and amelioration of inflammation. Increased serum levels of osteocalcin correlated inversely with BMI (r = −0.63; p < 0.001), total fat mass (r = −0.58, p < 0.001), total lean mass (r = −0.45, p < 0.001), C-reactive protein (CRP) (r = −0.37; p < 0.01), insulin (r = −0.4; p < 0.001), leptin (r = −0.53; p < 0.001), triglycerides (r = −0.42; p < 0.001), and alanine aminotransferase (ALAT) (r = −0.52; p < 0.001). Regression analysis revealed that osteocalcin was independently associated with changes in CRP but not with changes in insulin concentration, fat mass, or bone mineral density, suggesting that weight loss-induced higher serum osteocalcin is primarily associated with reduced inflammation.

Metabolic syndrome (MetS) is an association between obesity, dyslipidemia, hyperglycemia, hypertension, and insulin resistance. A relationship between MetS and vascular dementia was hypothesized. The purpose of this work is to investigate brain microanatomy alterations in obese Zucker rats (OZRs), as a model of MetS, compared to their counterparts lean Zucker rats (LZRs). 12-, 16-, and 20-weeks-old male OZRs and LZRs were studied. General physiological parameters and blood values were measured. Immunochemical and immunohistochemical techniques were applied to analyze the brain alterations. The morphology of nerve cells and axons, astrocytes and microglia were investigated. The blood–brain barrier (BBB) changes occurring in OZRs were assessed as well using aquaporin-4 (AQP4) and glucose transporter protein-1 (GLUT1) as markers. Body weight gain, hypertension, hyperglycemia, and hyperlipidemia were found in OZRs compared to LZRs. In the frontal cortex and hippocampus, a decrease of neurons was noticeable in the older obese rats in comparison to their age-matched lean counterparts. In OZRs, a reduction of neurofilament immunoreaction and gliosis was observed. The BBB of older OZRs revealed an increased expression of AQP4 likely related to the development of edema. A down-regulation of GLUT1 was found in OZRs of 12 weeks of age, whereas it increased in older OZRs. The behavioral analysis revealed cognitive alterations in 20-week-old OZRs. Based on these results, the OZRs may be useful for understanding the mechanisms through which obesity and related metabolic alterations induce neurodegeneration.

College students undergo stressors (e.g., potential financial strain, changes in workload or location), which may precipitate metabolic syndrome (MetS) risk associated with obesity and high blood pressure. Concerning rises in young adult obesity and type 2 diabetes, prompt study into MetS risk factor prevalence and awareness in youthful populations transitioning to new environments, such as college. This study assessed perceived stress, coping resources, and disease awareness differences in the first time on campus and final-year students associated with MetS risk factors (elevated body mass index (BMI) and blood pressure). We hypothesized lower stress perception, lower weight gain and blood pressure, higher MetS knowledge, and more positive coping strategies in final-year students. We conducted a longitudinal cohort study of 43 undergraduates with a baseline assessment in September (T0) and a follow-up in December (T1). BMI and blood pressure were measured at each visit and compared to baseline predictors of MetS knowledge, perceived stress, and coping resources. Though trends in MetS knowledge, perceived stress, and coping scores followed those in our hypothesis, only differences in weight and BMI change were statistically significant. The mixed-effects regression analysis did not find any statistically significant trends. First-time on-campus students gained an average of 1.736 kg, and their average BMI increased by 0.485 kg/m2. Conversely, final year students lost 0.313 kg, and their average BMI decreased by 0.210 kg/m2. Information on blood pressure was inconclusive. The average increase in weight/BMI in first-time on-campus students compared to final-year students highlights the need to provide education and resources to protect against metabolic syndrome risk in young adults. Trends in final year student clinical outcomes and their predictors illustrate how education may be a protective factor against MetS risk.

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