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Richard L Atkinson

Publications and source records attributed to Richard L Atkinson.

8 recordsLinked to original sources
PubMed2005

Adipogenic potential of multiple human adenoviruses in vivo and in vitro in animals.

Human adenovirus-36 (Ad-36) increases adiposity in chickens, mice, and nonhuman primates and is associated with human obesity. Ad-36 paradoxically reduces serum cholesterol and triglycerides in animal models. Ad-36 increases adipocyte differentiation and triglyceride accumulation in 3T3-L1 cells in vitro. This study evaluated whether three other human adenoviruses increase adiposity in chickens and in 3T3-L1 cells in vitro. We inoculated chickens with human Ad-2, Ad-31, Ad-37, or media at age 3 wk. Food intake and weights were recorded for 3.5 wk, and then chickens were killed and visceral fat, body composition, serum lipids, and viral antibody status were determined. Visceral fat and total body fat were significantly elevated (P < 0.001) in the Ad-37 group compared with all other groups. Final body weights were higher in chickens inoculated with Ad-37 compared with Ad-2, but not significantly higher than in control or Ad-31 groups. Food intake did not differ among groups. Serum cholesterol was elevated in Ad-37 chickens compared with control (P < 0.01) but was not affected by other viruses. Triglycerides were reduced in Ad-37 chickens (P < 0.0001) but were not affected by other viruses. In 3T3-L1 cells in vitro, Ad-31, Ad-36, and Ad-37, but not Ad-2, increased adipocyte differentiation and triglycerides accumulation. In summary, Ad-37 is another human adenovirus that increases adiposity and reduces serum triglycerides in an animal model. However, the response of serum cholesterol is opposite that of Ad-36. Evaluation of other human adenoviruses to determine their effects on adiposity and serum lipids is warranted, but in vitro assays may not be definitive for this purpose.

3T3-L1 Cells↗
PubMed2004

A human adenovirus enhances preadipocyte differentiation.

OBJECTIVE: Adenovirus 36 (Ad-36) has been shown to increase adiposity in experimentally infected chickens, mice, and marmosets (nonhuman primates). Neutralizing antibodies to Ad-36 are associated with obesity in humans. The metabolic and molecular mechanisms responsible for Ad-36-induced adipogenesis are unknown. As a potential adipogenic mechanism, this study examined if Ad-36 enhanced differentiation of preadipocytes. RESEARCH METHODS AND PROCEDURES: To determine the suitability of 3T3-L1 cells (murine preadipocyte cell line) as a model, the first experiment determined if Ad-36 attaches and initiates replication in the cells. Next, effects of Ad-36 on the number of differentiated adipocytes, glycerol 3-phosphate dehydrogenase (GPDH) levels, and cellular lipid accumulation were determined. The last experiment determined the effect of Ad-36 on human primary preadipocyte differentiation. Ad-2, a known nonadipogenic human adenovirus, was used as a negative control in these experiments. RESULTS: Immunofluorescence studies showed adenoviral attachment to 3T3-L1 cells, and reverse transcriptase-polymerase chain reaction showed expression of the Ad-36 E1A gene in the infected cells. Ad-36, but not Ad-2, increased the number of differentiated adipocytes, GPDH enzyme levels, and the total cellular lipid content. Also, Ad-36, but not Ad-2, increased GPDH levels in human preadipocytes. DISCUSSION: Taken together, these experiments showed that Ad-36 enhanced differentiation of preadipocytes, which may be a contributory mechanism to its adipogenic effect in vivo. The lack of effect of Ad-2 on differentiation demonstrated that the observed findings were not a common characteristic of all adenoviruses. Future understanding of the molecular interactions of cellular and viral genes responsible for enhanced differentiation may reveal novel signaling pathways and controls of preadipocyte differentiation.

3T3-L1 Cells↗
PubMed2003

Weight loss with self-help compared with a structured commercial program: a randomized trial.

CONTEXT: Although commercial weight loss programs provide treatment to millions of clients, their efficacy has not been evaluated in rigorous long-term trials. OBJECTIVE: To compare weight loss and health benefits achieved and maintained through self-help weight loss vs with a structured commercial program. DESIGN AND SETTING: A 2-year, multicenter randomized clinical trial with clinic visits at 12, 26, 52, 78, and 104 weeks conducted at 6 academic research centers in the United States between January 1998 and January 2001. PARTICIPANTS: Overweight and obese men (n = 65) and women (n = 358) (body mass index, 27-40) aged 18 to 65 years. INTERVENTION: Random assignment to either a self-help program (n = 212) consisting of two 20-minute counseling sessions with a nutritionist and provision of self-help resources or to a commercial weight loss program (n = 211) consisting of a food plan, an activity plan, and a cognitive restructuring behavior modification plan, delivered at weekly meetings. MAIN OUTCOME MEASURES: Weight change was the primary outcome measure. Secondary outcomes included waist circumference, body mass index, blood pressure, serum lipids, glucose, and insulin levels. RESULTS: At 2 years, 150 participants (71%) in the commercial group and 159 (75%) in the self-help group completed the study. In the intent-to-treat analysis, mean (SD) weight loss of participants in the commercial group was greater than in the self-help group at 1 year (-4.3 [6.1] kg vs -1.3 [6.1] kg, respectively; P<.001) and at 2 years (-2.9 [6.5] kg vs -0.2 [6.5] kg, respectively; P<.001). Waist circumference (P =.003) and body mass index (P<.001) decreased more in the commercial group. Changes in blood pressure, lipids, glucose, and insulin levels were related to changes in weight in both groups, but between-group differences in biological parameters were mainly nonsignificant by year 2. CONCLUSION: The structured commercial weight loss program provided modest weight loss but more than self-help over a 2-year period.

Adult↗
PubMed2003

Measurement of nutritional status in simulated microgravity by bioelectrical impedance spectroscopy.

The potential of bioelectrical impedance spectroscopy (BIS) for assessing nutritional status in spaceflight was tested in two head-down-tilt bed-rest studies. BIS-predicted extracellular water (ECW), intracellular water (ICW), and total body water (TBW) measured using knee-elbow electrode placement were compared with deuterium and bromide dilution (DIL) volumes in healthy, 19- to 45-yr-old subjects. BIS was accurate during 44 h of head-down tilt with mean differences (BIS - DIL) of 0-0.1 kg for ECW, 0.3-0.5 for ICW, and 0.4-0.6 kg for TBW (n = 28). At 44 h, BIS followed the within-individual change in body water compartments with a relative prediction error (standard error of the estimate/baseline volume) of 2.0-3.6% of water space. In the second study, BIS did not detect an acute decrease (-1.41 +/- 0.91 kg) in ICW secondary to 48 h of a protein-free, 800 kcal/day diet (n = 18). BIS's insensitivity to ICW losses may be because they were predominantly (65%) localized to the trunk and/or because there was a general failure of BIS to measure ICW independently of ECW and TBW. BIS may have potential for measuring nutritional status during spaceflight, but its limitations in precision and insensitivity to acute ICW changes warrant further validation studies.

Adult↗
PubMed2003

Prior exercise increases dietary oleate, but not palmitate oxidation.

OBJECTIVE: Higher levels of physical activity have been associated with body weight maintenance, but previous work in our laboratory suggests that this is not purely related to energy balance. We hypothesize that this may be related to the partitioning of dietary fat between oxidation and storage. RESEARCH METHODS AND PROCEDURES: Healthy women (age 24 +/- 1 years, BMI = 21.2 +/- 0.4 kg/m2) were recruited to participate in rest (n = 10) or exercise sessions of light (n = 11), moderate (n = 10), and heavy (n = 7) exercise. All exercises (1250 kJ above rest) were performed on a stationary cycle inside of a whole-body calorimeter. [1-(13)C]oleate and [d31]palmitate were given in a liquid meal 30 minutes post-exercise. An additional study was done with identical exercise sessions, but with administration of an oral dose of [1-(13)C]acetate and [d3]acetate 30 minutes post-exercise to determine label sequestration. RESULTS: Cumulative oxidation of [1-(13)C]oleate was significantly greater after light (45 +/- 3%), moderate (54 +/- 4%), and heavy (51 +/- 4%) exercise than that with rest (33 +/- 3%) (p = 0.0008). Cumulative oxidation of [d31]palmitate did not differ among trials (12 +/- 2%, 14 +/- 1%, 17 +/- 2%, and 14 +/- 2% for rest, light, moderate, and heavy, respectively; p = 0.30). DISCUSSION: Exercise standardized for energy expenditure increases monounsaturated fat oxidation more than saturated fat oxidation and that the increase occurs regardless of intensity. Recommendations for physical activity for the purposes of weight control may be specific for dietary fat composition.

Adult↗
PubMed2002

Human adenovirus Ad-36 promotes weight gain in male rhesus and marmoset monkeys.

Although obesity has multiple etiologies, an overlooked possibility is an infectious origin. We previously identified two viruses, SMAM-1, an avian adenovirus (Ad), and Ad-36, a human adenovirus, that produce a syndrome of visceral obesity, with paradoxically decreased serum cholesterol and triglycerides in chickens and mice. In the two studies presented in this paper, we used nonhuman primates to investigate the adiposity-promoting potential of Ad-36. In study 1, we observed spontaneously occurring Ad-36 antibodies in 15 male rhesus monkeys, and a significant longitudinal association of positive antibody status with weight gain and plasma cholesterol lowering during the 18 mo after viral antibody appearance. In study 2, which was a randomized controlled experiment, three male marmosets inoculated with Ad-36 had a threefold body weight gain, a greater fat gain and lower serum cholesterol relative to baseline (P <0.05) than three uninfected controls at 28 wk postinoculation. These studies illustrate that the adiposity-promoting effect of Ad-36 occurs in two nonhuman primate species and demonstrates the usefulness of nonhuman primates for further evaluation of Ad-36-induced adiposity.

Adenoviridae Infections↗
PubMed2002

Prior exercise increases subsequent utilization of dietary fat.

PURPOSE: Exercise appears to offer protection against weight gain, perhaps related to its effects on fat metabolism. Previous work in rats has shown that interventions resulting in a negative energy balance lead to alterations in the trafficking of dietary fat. This study was undertaken to determine whether exercise after an overnight fast would alter the partitioning of dietary fat between oxidation and storage. METHODS: Seven female subjects (age = 26 +/- 1 yr, BMI = 21 +/- 1 kg x m(-2); mean +/- SEM) were recruited for three visits: rest, light, and heavy exercise. Stationary cycle exercise sessions were calculated to use 1,250 kJ and were done in a whole-body calorimeter. Dietary fat oxidation was calculated from the recovery of (13)C-oleate corrected for acetate sequestration and d(31)-palmitate given in a liquid meal 30 min after the completion of exercise. RESULTS: Cumulative oxidation of (13)C-oleate at 11.5 h postdose was significantly greater during the heavy exercise (49 +/- 4%) trial than both the light exercise (39 +/- 4%) and the rest trials (34 +/- 4%) (P < 0.005). Oxidation of d(31)-palmitate recovery at 11.5 h postdose was not different during the heavy exercise (12 +/- 1%), light exercise (11 +/- 1%), and rest trials (10 +/- 1%). CONCLUSIONS: These data illustrate that exercise has the ability to alter the trafficking of dietary fat. Furthermore, the effect of exercise is dependent on the type of fatty acid.

Adult↗