Home environment and psychosocial predictors of obesity status among community-residing men and women.

BACKGROUND/OBJECTIVES: Prior research indicates that features of the home environment (for example, televisions, exercise equipment) may be associated with obesity, but no prior study has examined objective features of the home food environment (for example, location of food) in combination with behavioral (for example, food purchasing), psychological (for example, self-efficacy) and social factors among obese adults. This study identified factors associated with obesity status from measures of home environment, food purchasing behavior, eating behavior and psychosocial functioning. SUBJECTS/METHODS: One hundred community-residing obese (mean body mass index (BMI)=36.8, s.e.=0.60) and nonobese (mean BMI=23.7, s.e.=0.57) adults (mean age=42.7, s.e.=1.50; range=20-78 years) completed an observational study with 2-h home interview/assessment and 2-week follow-up evaluation of food purchases and physical activity. Data were analyzed with analysis of variance and logistic regression, controlling for sex. RESULTS: Univariate analyses revealed that homes of obese individuals had less healthy food available than homes of nonobese (F(1,97)=6.49, P=0.012), with food distributed across a greater number of highly visible locations (F(1,96)=6.20, P=0.01). Although there was no group difference in household income or size, obese individuals reported greater food insecurity (F(1,97)=9.70, P<0.001), more reliance on fast food (F(1,97)=7.63, P=0.01) and more long-term food storage capacity in number of refrigerators (F(1,97)=3.79, P=0.05) and freezers (F(1,97)=5.11, P=0.03). Obese individuals also reported greater depressive symptoms (F(1,97)=10.41, P=0.002) and lower ability to control eating in various situations (F(1,97)=20.62, P<0.001). Multiple logistic regression revealed that obesity status was associated with lower self-esteem (odds ratio (OR) 0.58, P=0.011), less healthy food consumption (OR 0.94, P=0.048) and more food available in the home (OR 1.04, P=0.036). CONCLUSIONS: The overall pattern of results reflected that home food environment and psychosocial functioning of obese individuals differed in meaningful ways from that of nonobese individuals. In particular, lower self-esteem may be an important psychosocial aspect of obesity, especially in the context of greater food consumption and food storage/availability.

Measurement of the rate of entry of intact colon-derived lactose into the circulation: a model for assessing gut uptake of molecules not endogenously synthesized.

BACKGROUND: Results of in vitro studies have documented colonic absorption of lactose in the newborn. A stable isotope model was developed for assessing the entry rate of intact lactose into the portal circulation in newborn piglets. METHODS: In experiment 1, unlabeled and [D-1-(13C)]-lactose were infused into two separate mesenteric veins, and in experiment 2, labeled lactose was infused into a mesenteric vein and unlabeled lactose was infused into the colon. The 13C-enrichment of plasma lactose was assessed by high performance liquid chromatography gas chromatography combined with mass spectrometry. RESULTS: The isotopic estimate of the mesenteric venous infusion rate of lactose was 91% of the theoretical. In the second experiment 13% of the unlabeled lactose infused into the colon reached the portal circulation. CONCLUSIONS: The current study provides the first, direct, in vivo confirmation of colon absorption of intact lactose. The tracer model could be used to evaluate intestinal or colonic absorption of other organic compounds not endogenously synthesized, including vitamins or drugs.

Effect of endurance training on hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men.

In humans, endurance training markedly reduces the rate of hepatic glucose production during exercise. To determine whether this is due to a reduction in glycogenolysis, in gluconeogenesis, or in both processes, six men were studied at rest and during 2 h of cycle ergometer exercise at 60% pretraining peak O2 consumption (VO2peak), both before and after completion of a strenuous endurance training program (cycling at 75-100% VO2peak for 45-90 min/day, 6 days/wk for 12 wk). The overall rate of glucose appearance (Ra) was determined using a primed continuous infusion of [6,6-2H]glucose, whereas the rate of gluconeogenesis (Rgng) was estimated from the incorporation of 13C into glucose (via pyruvate carboxylase) from simultaneously infused [13C]bicarbonate. Training did not affect glucose kinetics at rest but reduced the average Ra during exercise by 42% [from 36.8 +/- 3.8 to 21.5 +/- 3.6 (SE) mumol.min-1.kg-1; P < 0.001]. This decrease appeared to be mostly due to a reduction in hepatic glycogenolysis. However, the estimated Rgng during exercise also decreased significantly (P < 0.001) with training, falling from 7.5 +/- 1.6 mumol.min-1.kg-1 (23 +/- 3% of total Ra) before training to 3.1 +/- 0.6 mumol.min-1.kg-1 (14 +/- 3% of total Ra) after training. These training-induced adaptations in hepatic glucose metabolism were associated with an attenuated hormonal response to exercise (i.e., higher insulin and lower glucagon, norepinephrine, and epinephrine concentrations) as well as a reduced availability of gluconeogenic precursors (i.e., lower lactate and glycerol concentrations). We conclude that endurance training reduces both hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men.

Ten days of exercise training reduces glucose production and utilization during moderate-intensity exercise.

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.

Isotopic estimation of CO2 production during exercise before and after endurance training.

Endurance training reduces the rate of CO2 release (i.e., VCO2) during submaximal exercise, which has been interpreted to indicate a reduction in carbohydrate oxidation. However, decreased ventilation, decreased buffering of lactate, and/or increased fixation of CO2 could also account for a lower VCO2 after training. We therefore used a primed continuous infusion of NaH13CO3 to determine the whole body rate of appearance of CO2 (RaCO2) in seven men during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2peak) before and after endurance training. RaCO2 is independent of the above-described factors affecting VCO2 but may overestimate net CO2 production due to pyruvate carboxylation and subsequent isotopic exchange in the tricarboxylic acid cycle. Training consisted of cycling at 75-100% VO2peak for 45-90 min/day, 6 days/wk, for 12 wk and increased VO2peak by 28% (P < 0.001). VCO2 during submaximal exercise was reduced from 86.8 +/- 3.7 to 76.2 +/- 4.2 mmol/min, whereas RaCO2 fell from 88.9 +/- 4.0 to 76.4 +/- 4.4 mmol/min (both P < 0.001). VCO2 and RaCO2 were highly correlated in the untrained (r = 0.98, P < 0.001) and trained (r = 0.99, P < 0.001) states, as were individual changes in VCO2 and RaCO2 with training (r = 0.88, P < 0.01). These results support the hypothesis that endurance training decreases CO2 production during exercise. The magnitude and direction of this change cannot be explained by reported training-induced alterations in amino acid oxidation, indicating that it must be the result of a decrease in carbohydrate oxidation and an increase in fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium chlorite administration in Long-Evans rats: reproductive and endocrine effects.

Long-Evans rats, 4-6 weeks of age, were given access to 0, 1, 10, or 100 ppm sodium chlorite in deionized water ad libitum as drinking water. Males were exposed 56 days, and females for 14 days prior to breeding and throughout the 10-day breeding period. Males were evaluated for sperm parameters and reproductive tract histopathology following the breeding period. Females were exposed throughout gestation and lactation. Dams and pups were necropsied at weaning. Decreases in serum T3 and T4 were observed on Postnatal Days 21 and 40 in male and female pups exposed to 100 ppm chlorite or above. Additionally, groups of males were exposed to 0, 10, 100, or 500 ppm ad libitum in the drinking water to confirm observed subtle reproductive effects and examine dose-effect relationships. A significant increase in the percentage of abnormal sperm morphology (P less than 0.001) and decrease in sperm direct progressive movement (P less than 0.01) were observed for adult males at chlorite levels of 100 or 500 ppm. Since other clinical and reproductive endpoints were not affected, sperm morphology and sperm direct progressive movement may be two of the more sensitive indicators of reproductive damage.