Effects of Walking Speed on Total and Regional Body Fat in Healthy Postmenopausal Women

Introduction: This study had two aims: (1) To confirm the efficacy of exercise speed and impulse (session duration at a given speed) to produce total and abdominal fat loss in postmenopausal women, and (2) compare the exercise speed and impulse necessary for the stimulation of fat loss to the suppression of bone mineral loss. Of special interest was to compare these parameters of exercise on fat loss in the same study and with the same subjects where they were found to suppress bone mineral loss. We hypothesized that (1) more total fat will be lost with slow walking and a longer impulse than with fast speed and shorter impulse, and (2) more abdominal subcutaneous (SC) and visceral fat (VF) will be lost with fast walking speed. Materials and Methods: Fat loss and suppression of bone mineral loss were measured in the same 25 subjects after 15 weeks, and fat measurements were also taken after 30 weeks in 16 residual subjects. Study parameters were walking a 4.8 km distance 4 days/week at either 6.6 km/h (120% of ventilatory threshold (VT)) or at 5.5 km/h (101.6% of VT) and expending 300 kcal/session. Body composition (fat and lean body mass, LBM) was measured with dual-energy X-ray absorptiometry (DXA) and anthropometric methods. Results: Slow walkers in the residual group progressively lost a significant percent of total body fat over 30 weeks while no such loss occurred after 15 weeks in fast walkers in either group, supporting hypothesis 1. However, the 20% higher starting body fat in 16 residual slow relative to fast subjects suggests that exercise fat loss is greater in overweight than in lean subjects. In fast walkers, fat loss occurred after 30 weeks of training. Hypothesis 2 was not supported as both speeds led to equal VF loss in 30-week group as estimated by waist circumference (CF) confirming that VF responds to the magnitude of energy expenditure and not the walking speed. Conclusions: Total body fat is lost through walking at all speeds, but the change is more rapid, clear, and initially greater with slow walking in overweight subjects. A longer exercise impulse at a lower speed in our study initially produced greater total fat loss than a shorter one with fast walking speed. This was reversed in comparison to how the same exercise in the same subjects suppressed bone mineral loss. Data from other studies indicate that longer impulses may promote greater fat loss at both slow and high exercise speeds, and our study providing only a 4.8 km walking distance may have limited the walking impulse and the magnitude of fat loss. Increased exercise energy expenditure at either walking speed produces equivalent declines in visceral fat in postmenopausal women, and with sufficiently long impulses, should reduce disabilities associated with central obesity.     

Interaction of normal and expanded CAG repeat sizes influences age at onset of Huntington disease

Huntington disease (HD) is a neurodegenerative disorder caused by the abnormal expansion of CAG repeats in the HD gene on chromosome 4p16.3. Past studies have shown that the size of expanded CAG repeat is inversely associated with age at onset (AO) of HD. It is not known whether the normal Huntington allele size influences the relation between the expanded repeat and AO of HD. Data collected from two independent cohorts were used to test the hypothesis that the unexpanded CAG repeat interacts with the expanded CAG repeat to influence AO of HD. In the New England Huntington Disease Center Without Walls (NEHD) cohort of 221 HD affected persons and in the HD-MAPS cohort of 533 HD affected persons, we found evidence supporting an interaction between the expanded and unexpanded CAG repeat sizes which influences AO of HD (P = 0.08 and 0.07, respectively). The association was statistically significant when both cohorts were combined (P = 0.012). The estimated heritability of the AO residual was 0.56 after adjustment for normal and expanded repeats and their interaction. An analysis of tertiles of repeats sizes revealed that the effect of the normal allele is seen among persons with large HD repeat sizes (47-83). These findings suggest that an increase in the size of the normal repeat may mitigate the expression of the disease among HD affected persons with large expanded CAG repeats.     

Inflammatory Effects of Edwardsiella ictaluri Lipopolysaccharide Modifications in Catfish Gut

Bacterial lipopolysaccharides (LPS) are structural components of the outer membranes of Gram-negative bacteria and also are potent inducers of inflammation in mammals. Higher vertebrates are extremely sensitive to LPS, but lower vertebrates, like fish, are resistant to their systemic toxic effects. However, the effects of LPS on the fish intestinal mucosa remain unknown. Edwardsiella ictaluri is a primitive member of the Enterobacteriaceae family that causes enteric septicemia in channel catfish (Ictalurus punctatus). E. ictaluri infects and colonizes deep lymphoid tissues upon oral or immersion infection. Both gut and olfactory organs are the primary sites of invasion. At the systemic level, E. ictaluri pathogenesis is relatively well characterized, but our knowledge about E. ictaluri intestinal interaction is limited. Recently, we observed that E. ictaluri oligo-polysaccharide (O-PS) LPS mutants have differential effects on the intestinal epithelia of orally inoculated catfish. Here we evaluate the effects of E. ictaluri O-PS LPS mutants by using a novel catfish intestinal loop model and compare it to the rabbit ileal loop model inoculated with Salmonella enterica serovar Typhimurium LPS. We found evident differences in rabbit ileal loop and catfish ileal loop responses to E. ictaluri and S. Typhimurium LPS. We determined that catfish respond to E. ictaluri LPS but not to S. Typhimurium LPS. We also determined that E. ictaluri inhibits cytokine production and induces disruption of the intestinal fish epithelia in an O-PS-dependent fashion. The E. ictaluri wild type and ΔwibT LPS mutant caused intestinal tissue damage and inhibited proinflammatory cytokine synthesis, in contrast to E. ictaluri Δgne and Δugd LPS mutants. We concluded that the E. ictaluri O-PS subunits play a major role during pathogenesis, since they influence the recognition of the LPS by the intestinal mucosal immune system of the catfish. The LPS structure of E. ictaluri mutants is needed to understand the mechanism of interaction.