Eat better & move more: a community-based program designed to improve diets and increase physical activity among older Americans.

OBJECTIVES: We assessed outcomes of an integrated nutrition and exercise program designed for Older Americans Act Nutrition Program participants as part of the Administration on Aging's You Can! campaign. METHODS: A 10-site intervention study was conducted. Preintervention and postintervention assessments focused on nutrition and physical activity stages of change, self-reported health status, dietary intakes, physical activity, and program satisfaction. RESULTS: Of 999 enrollees, the 620 who completed the program were aged 74.6 years on average; 82% were women, and 41% were members of racial/ethnic minority groups. Factors associated with program completion were site, health conditions, and nutrition risk. Seventy-three percent and 75% of participants, respectively, made a significant advance of 1 or more nutrition and physical activity stages of change; 24% reported improved health status. Daily intake of fruit increased 1 or more servings among 31% of participants; vegetables, 37%; and fiber, 33%. Daily steps increased 35%; blocks walked, 45%; and stairs climbed, 24%. Program satisfaction was 99%. CONCLUSIONS: This easy-to-implement program improves diets and activity levels. Local providers should offer more such programs with the goal of enabling older Americans to take simple steps toward successful aging.

Continuous low-dose fructose infusion does not reverse glucagon-mediated decrease in hepatic glucose utilization.

An adaptation to continuous total parenteral nutrition (TPN; 75% of nonprotein calories as glucose) is the liver becomes a major consumer of glucose with lactate release as a by-product. The liver is able to further increase liver glucose uptake when a small dose of fructose is acutely infused via the portal system. Glucagon, commonly elevated during inflammatory stress, is a potent inhibitor of glucose uptake by the liver during TPN. The aim was to determine if continuous fructose infusion could overcome the glucagon-mediated decrease in hepatic glucose uptake. Studies were performed in conscious, insulin-treated, chronically catheterized, pancreatectomized dogs that adapted to TPN for 33 hours. They were then assigned to 1 of 4 groups: TPN (C), TPN + fructose (4.4 µmol kg(-1) min(-1); F), TPN + glucagon (0.2 pmol kg(-1) min(-1); GGN), or TPN + fructose and glucagon (F + GGN) for an additional 63 hours (33-96 hours). Insulin, fructose, and glucagon were infused into the portal vein. During that period, all animals received a fixed insulin infusion of 0.4 mU·kg(-1)·min(-1) (33-96 hours); and the glucose infusion rates were adjusted to maintain euglycemia (6.6 mmol/L). Continuous fructose infusion was unable to further enhance net hepatic glucose uptake (in micromoles per kilogram per minute) (31.1 ± 2.8 vs 36.1 ± 5.0; C vs F), nor was it able to overcome glucagon-mediated decrease in net hepatic glucose uptake (10.0 ± 4.4 vs 12.2 ± 3.9; GGN vs F + GGN). In summary, continuous fructose infusion cannot augment liver glucose uptake during TPN; nor can it overcome the inhibitory effects of glucagon.

COX-2 inhibition attenuates anorexia during systemic inflammation without impairing cytokine production.

Anorexia and weight loss are frequent complications of acute and chronic infections and result from induction of cytokines, prostaglandins, and other inflammatory mediators that are critical for pathogen elimination. Selective attenuation of the hypophagic response to infection and maintenance of the production of factors essential for infection control would be a useful addition to antimicrobial therapy in the treatment of human disease. Here, we evaluate the relative contribution of cyclooxygenase (COX)-1- and COX-2-derived prostaglandins to anorexia and weight loss precipitated by systemic immune activation by lipopolysaccharide (LPS). Using COX isoform-selective pharmacological inhibitors and gene knockout mice, we found that COX-2 inhibition during LPS-induced inflammation results in preserved food intake and maintenance of body weight, whereas COX-1 inhibition results in augmented and prolonged weight loss. Regulation of neuropeptide Y, corticotropin-releasing hormone, leptin, and interleukin-6 does not change as a function of COX-2 inhibition after LPS administration. Our data implicate COX-2 inhibition as a therapeutic target to maintain nutritional status while still allowing a normal cytokine response during infection.