No Differences in Energy Cost of a Predetermined Exercise among Young Overweight/Obese and Undernourished Individuals.

BACKGROUND: Physical activity is an integral part of one's daily life. Obese (Ob) and undernourished (UN) persons are known to underperform physically as compared to normal weight (N) individuals. In this study, we have measured the energy spent to perform a prefixed exercise on treadmill walking and basal heart rate and blood pressure. Body mass index (BMI) and body fat of participating individuals were assessed. Fasting blood sugar and lipid profile were also evaluated. MATERIALS AND METHODS: Eighty-three young individuals (male: 41; female: 42) of medical faculty, Universiti Sultan Zainal Abidin, who volunteered for the study, were recruited. The mean age of the individuals was 19.8 ± 0 years (P < 1.08). The individuals were grouped as N, UN/underweight, and overweight (Ow)/Ob based on BMI. RESULTS: The results of the study revealed that there were no differences in the energy spent on performing the predetermined treadmill walking of 20 min duration among the three groups (a mean of 78 and 70 calories in all male and female subgroups, respectively). The distance covered by the males was 1.6 km while the females covered 1.4 km on treadmill walking in 20 min time. Basal blood pressure and heart rate and fasting blood sugar did not reveal any significant difference among the groups. However, total cholesterol and triglyceride levels were marginally higher in the Ow/Ob groups of male and female individuals as compared to other groups. CONCLUSION: Since the study individuals were very young and competitive by nature and possibly had no major metabolic disturbances, the differences in physical activity performances were not obvious. Possibly, such differences would become apparent only at later stages of life as age advances or when the intensity and duration of exercise are set at higher levels.

Recent advances in human brown fat physiology.

Of the two variants of adipose tissue, white fat is traditionally known as a lipid rich tissue which undergoes pathological expansion in obese conditions. To counter the excess accumulation of white fat in states of energy imbalance, the second and unique type of brown fat plays a key role by burning extra energy into heat through a special metabolic pathway. In addition brown fat also plays a vital role in thermoregulation in animals and newborn humans and infants. Recent progress in research areas of these two types of fat tissue has provided compelling evidence to show that they secrete a large number of chemicals that play an important role in body weight control that involves several mechanisms. Brown fat was considered absent in the adult humans until recently. But new techniques have provided ample support for its active existence. Based on the very recent data it has been suggested that brown fat can be a target organ in the treatment of obesity which can lead to exciting and informative outcomes in the future.

Differing response of body weight gain to high fat diet treatment in the mouse.

Forty-eight mice maintained on a high fat diet supplement in addition to regular laboratory rodent chow responded differently in terms of body weight gain over a period of six weeks. Eleven mice gained weight that was comparable to body weights of mice given only chow for the same period of time while the others gained significantly higher body weights and became obese despite similar level of energy intakes. The increase in body weight was due to increase in body fat content as noted by carcass analysis. The differential response of the mice to identical dietary treatment in causing obesity or not in mice is discussed.

Body fat and lean body mass assessment in human subjects--a comparison of two different techniques.

Body fat and lean body mass was assessed in young college students by two different techniques involving NIR method and body circumference measurements. NIR technique significantly over-estimated the body fat as compared to the results obtained by the other method. The difference between the methods was 23-30% high for fat and the variation was 5-9% low for lean body mass for the whole group. Results obtained by the body girth size measurements agreed well with fat and lean body mass values from other studies on Indian subjects which had employed different methods.

Effects of ethanol consumption on brown adipose tissue thermogenic capacity in mice.

The objective of this work was to evaluate the effects of ethanol consumption on brown adipose tissue (BAT) thermogenic capacity in mice. Mice offered only ethanol (10%; v/v) for 10 days as drinking fluid had significant reductions in total energy and fluid intakes relative to mice given water, but net weight gains were similar. BAT thermogenic capacity was reduced in mice drinking ethanol, as shown by decreases in tissue protein and succinate dehydrogenase (SDH) activity and in the uncoupling protein content of isolated mitochondria. Ethanol consumption differed greatly between mice offered a choice between ethanol and water for 25 days after a 10-day habituation period, with only ethanol as the drinking solution. Total energy intake of mice that continue to consume the most ethanol voluntarily (up to 25% of total fluid intake) was significantly reduced but carcass fat was increased, relative to mice consuming less or no ethanol. Brown fat thermogenic capacity was not significantly affected by the degree of ethanol consumption. Basal and norepinephrine-stimulated rates of oxygen uptake of isolated brown adipocytes were not affected by ethanol. Thus, changes in the animal capacity for energy expenditure in brown adipose tissue does not appear an important factor to explain the effects of ethanol consumption on fat deposition in mice.

Alcohol dehydrogenase activity in mouse brown adipose tissue.

The present work provides evidence for the occurrence of the enzyme alcohol dehydrogenase (ADH) in very minute concentration in mice brown adipose tissue (BAT). Mice consuming 10% ethanol for 10 days showed significantly lowered enzyme activity in brown fat while liver ADH activity was increased but not significantly. Measurements of basal and norepinephrine stimulated oxygen consumption of isolated brown adipocytes indicated that the presence of ADH in BAT of mice is unlikely to play any role in ethanol oxidation.

Metabolic responses to episodes of partial dietary restriction in undernourished Wistar rats.

Wistar rat pups raised in large litters (LL) and small litters (SL) prior to weaning had access to ad libitum dietary intakes up to the age of 90 days. At 90 and again at 180 days they were partially diet restricted for a period of 15 days. Body weights, resting metabolic rates (RMR) and capacity for nonshivering thermogenesis (NST) was evaluated prior to, during and after the period of energy restriction. Responses were compared with 180 day rats from both groups who had been diet restricted for the first time at 180 days. Body weight losses were greater in the latter group. Groups of rats exposed to dietary restriction once, had higher body weights than rats of identical ages who had not been restricted. RMR decreased in all groups during restriction. However, reductions in NST were seen only in nutritionally deprived animals and in well-nourished controls who were partially restricted once. Changes in NST contribute to metabolic efficiency seen during episodic dietary restriction.

Changes in brown adipose tissue composition during fasting and refeeding of diet-induced obese mice.

The objective of this work was to evaluate how obesity would influence the changes in brown fat (BAT) thermogenic capacity during fasting-refeeding. Mice fed either chow or chow + high-fat supplement for 6 wk had body weights of 34 +/- 1 and 43 +/- 1 g, respectively. They were fasted for 48 h followed by ad libitum refeeding for up to 5 days. Loss of carcass fat was similar between food-deprived mice previously fed chow or chow + high-fat supplement. However, even after a 48-h fast, obese mice still had a carcass fat content much greater than that of chow-fed mice. Brown fat atrophy caused by food deprivation was characterized by reductions in tissue weight, fat, mitochondrial proteins and uncoupling protein (UCP), without change in tissue DNA. Obesity did not alter the rate or extent of brown fat atrophy. Upon refeeding 48-h-fasted lean and obese mice, there was recovery of BAT thermogenic capacity that was similar between the two groups. In chow-fed mice, an intact neural input was essential for recovery of BAT thermogenic capacity during refeeding. These results indicate that food deprivation triggers an immediate adaptive response in mice previously fed chow or chow + a high-fat supplement and that reduction in brown fat thermogenic capacity during fasting and its recovery during refeeding appear little affected by the size of the animal energy reserves.

Role of mast cell histamine in brown adipose tissue thermogenic response to VMH stimulation.

Electrical stimulation of the ventromedial hypothalamic area in rats caused a significant but transient increase in interscapular brown adipose tissue temperature. This response was markedly reduced by cimetidine, a histamine H2-receptor antagonist, but not by pyrilamine, an H1-receptor antagonist. Histamine is present in substantial amounts within mast cells in brown adipose tissue as injections of compound 48/80, which cause degranulation of connective tissue mast cells, reduced the tissue histamine content by > 85%. In contrast, histamine content in brown adipose tissue was not affected by loss of sympathetic neural input (with 6-hydroxydopamine) or sensory neural input (with capsaicin). Neither cimetidine nor histamine had any effect on basal and norepinephrine-stimulated rates of O2 consumption by isolated brown adipocytes. These results indicate that histamine released from mast cells acting on H2-receptors may play an important but indirect role in the thermogenic response of brown adipose tissue to stimulation of the ventromedial hypothalamic area.

The impact of early undernutrition on voluntary food consumption in later life of rats.

Food consumption patterns were studied during ad-libitum feeding of rats undernourished for 21 or 60 days after birth. Rats undernourished for 21 days consumed less food than the controls on a whole animal basis. But the food intake was higher during the early part of ad-libitum feeding when expressed on a unit body weight or metabolic body weight basis, and subsequently became comparable to that of the controls. Male rats undernourished for 60 days showed either comparable (for the whole animal) or higher (in other terms) food consumption, whereas the female rats undernourished for 60 days consumed more food at the beginning of ad-libitum feeding but less food during the latter part, when compared to their respective controls. The results thus indicate that no single mechanism can completely explain the food intake of undernourished rats during nutritional rehabilitation.

Sucrose feeding stimulates basal metabolism & nonshivering thermogenesis in undernourished rats.

Undernutrition in rats for 60 days from the first day of birth resulted in a significant diminution of nonshivering thermogenesis (NST) and basal metabolic rate (BMR; 12.5 and 5% respectively) as compared to their controls, even when expressed on a metabolic body weight basis. Sucrose (8%) feeding for 72 h of such undernourished (UN) rats immediately after 60 days reverted the depressed NST capacity to levels comparable to control values while the BMR was higher by about 9 per cent than controls. The actual increase in NST and BMR of UN rats after 72 h of sucrose feeding was about 12 and 14 per cent respectively when compared to the values before sucrose feeding. This is possibly because sucrose feeding is known to elevate the caloric intake by 20-30 per cent over normal and would stimulate the sympathetic nervous system (SNS) activity. The results thus would imply that the reduced NST and BMR in rats consequent to undernutrition is probably due to diminished SNS activity which may be associated with changes in some hormonal and brown adipose tissue functions. However, such changes appear to be limited only to the period of undernutrition as it can be corrected speedily by adequate energy supplementation.

Basal metabolic rate, nonshivering thermogenesis and cold tolerance in rat during undernutrition and subsequent nutritional rehabilitation.

Nutritional deprivation induced by increasing the litter size and subsequent dietary restriction results in rats having lower body weights and body lengths. Such undernourished rats have lower body temperatures as well as lower basal metabolic rate and nonshivering thermogenesis on a metabolic body weight basis; they also succumb on cold exposure to 5 degrees C. Nutritional rehabilitation by access to unlimited food reverses these changes to levels comparable to their control values.

Nutritional status and spontaneous locomotor activity in the rat.

A considerable amount of energy may be saved by lowering the spontaneous locomotor activity when energy intakes are reduced. The results of the present study in rats undernourished for a period of 21 or 60 days and subsequently fed ad libitum diet did not show any differences in activity when compared to their respective control groups, either during the undernourished periods or well fed states. Although this would mean that the rats are not economising energy on activity, it is probable that these rats with lower body weights are contributing to energy saving mechanism by reducing the cost of activity per se since the cost of activity and body weight are directly related.

Cold-induced thermogenesis in rats nutritionally deprived early in life.

Preweaning nutritional deprivation with or without postweaning partial energy restriction produces animals of small size with defective nonshivering thermogenesis. This is also associated with their inability to tolerate cold exposure to 5 degrees C. Adequate nutritional rehabilitation for a reasonable length of time of 10 days abolishes the defect in cold induced thermogenesis (CIT) although the deficits in body weight or body size are not corrected. This may indicate that the defect may be possibly due to the non availability of enough substrates rather than to a change in the functioning of thermogenic organs such as brown adipose tissue. Sucrose feeding which enhances caloric intake and hence sympathetic activity can reverse the defect in CIT only in older rats suggesting the possibility of delayed maturation of thermoregulatory functions in young rats which are energy deprived. The results of this study possibly indicate that there may be a temporary reduction of the sympathetic nervous system activity during the period of energy restriction which compromises cold tolerance and which is reactivated rapidly following nutritional rehabilitation.

Effects of preweaning nutritional deprivation on basal metabolism and thermoregulatory thermogenesis in the rat.

1. Nutritional deprivation was induced preweaning in Wistar rats by increasing the litter size to sixteen, while paired litters with only five pups served as controls. The nutritionally deprived pups were rehabilitated after weaning by ad lib. access to an adequate diet. 2. The body-weights and body lengths were significantly lower in the nutritionally deprived group and significant differences persisted even after 9 weeks of rehabilitation. 3. The body temperature of the nutritionally deprived animals was significantly lower than that of their paired controls, both before and following nutritional rehabilitation, except for a short period after weaning when the nutritionally deprived animals were initially given the diet ad lib. 4. The resting oxygen consumption of the nutritionally deprived animals was comparable to that of the controls when corrected for metabolic body size, both before and after weaning. Noradrenaline-stimulated increase in O2 consumption (non-shivering thermogenesis; NST) was reduced by 50% at weaning in the nutritionally deprived animals and returned to levels comparable to those of controls within a short period of rehabilitation. 5. The decrease in NST capacity seen in the nutritionally deprived animals was associated with an inability to thermoregulate when exposed to cold (5 degrees), resulting in death. Cold-induced thermogenesis (CIT) also reappeared soon after nutritional rehabilitation. 6. Reduction in metabolic rate, NST and CIT seen in the animals nutritionally deprived preweaning was short-lived and disappeared soon after nutritional rehabilitation. Rapid reversal of these physiological changes indicates that they do not confer any long-term benefit or change in metabolic efficiency and are unlike the changes in body size and growth which do not completely recover following nutritional rehabilitation.

A closed circuit apparatus for measurement of oxygen consumption in small animals.

A simple and reliable closed circuit apparatus for short term and long term measurements of oxygen consumption of small laboratory animals is described. Repeat measurements of oxygen consumption under resting conditions of six male albino rats using this apparatus shows a variability of less than 1.5%. Use of the set-up for continuous monitoring of oxygen consumption following subcutaneous injection of norepinephrine, for over 2.5 hr enables the measurement of energy expenditure in animals on a long term basis which is reproducible on several occasions.