Changes in Adipose Mass and Cellularity Through the Adult Life of Rats Fed Ad Libitum or a Life-Prolonging Restricted Diet

Bertrand, Helen A.; Lynd, Frederick T.; Masoro, Edward J.; Yu, Byung P.

doi:10.1093/geronj/35.6.827

Cited by 192 publications

(101 citation statements)

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“…The increase of body fat percentage seems to occur even in animals fed an energy-restricted diet, if this diet contains energy sufficient for maintaining body weight (29). This fact also was recognized in the present study.…”

Section: Discussionsupporting

confidence: 85%

Long-term effect of energy restriction at different protein levels on several parameters of nutritional assessment.

Rikimaru

Ichikawa

Oozeki

et al. 1988

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryExperiments were conducted to evaluate long-term effects of energy restricted diets containing different protein levels initiated in adult life on various parameters of nutritional assessment . Rats (male SPF Wistar) were fed 20%-casein diet ad libitum, or 10%-, 20%-, or 40%-casein diets (group 10R, 20R, and 40R, respectively) under energy-restricted conditions, which corresponded to about 60% ad libitum feeding , from 18 to 55 weeks of age. Energy restriction induced a decrease of body-lipid percentage. Although skeleton weight and tail length increased through out the experimental period in all the groups, these increases were found to be depressed under energy restriction. On the other hand, protein intake level under the energy restriction did influence plasma concentrations of urea and cholesterol, hematocrit, and systolic blood pressure. The group fed the 40%-casein diet tended to be lower in total cholesterol levels at 55 weeks of age, while the group fed 10%-casein diet tended to be lower in hematocrit and higher in systolic blood pressure levels . When mature rats were fed the 60%-energy-restricted diet for a long-term period , those on the 20% and 40%-casein diets showed somewhat more preferable levels of hematocrit and blood pressure than those on the 10%-casein diet; the 10%-casein diet did not, however, reveal symptoms of malnutrition .

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Section: Discussionsupporting

confidence: 85%

Long-term effect of energy restriction at different protein levels on several parameters of nutritional assessment.

Rikimaru

Ichikawa

Oozeki

et al. 1988

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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show abstract

“…Such a conclusion may not be correct, however, in view of the data from a previous study on body composition of AL and DR rats. Our earlier work (2) showed that, during the period of life prior to the beginning of terminal weight loss, the body fat content of the AL rats averaged 17% of body weight, a value that was much greater than the 11% body fat content found in the DR rats. In addition, body fat was markedly decreased during terminal weight loss before a reduction in lean body mass was observed (2,33).…”

Section: Discussionmentioning

confidence: 78%

Senescent terminal weight loss in the male F344 rat

Black¹,

McMahan²,

Masoro

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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. Senescent terminal weight loss in the male F344 rat. Am J Physiol Regul Integr Comp Physiol 284: R336-R342, 2003. First published October 17, 2002 10.1152/ajpregu.00640.2001.-Loss of weight, often of unknown cause and culminating in death, commonly occurs in humans at advanced ages. Rats that live to old ages, such as the Fischer 344 (F344) strain, also exhibit a terminal loss in body weight. A presently held hypothesis is that the terminal weight loss in the F344 rat model is due to reduced food intake because of an alteration in hypothalamic function resulting in early satiation. We report findings on terminal weight loss and food intake in male F344 rats fed ad libitum (AL group) or a life-prolonging dietary regimen in which caloric intake was restricted (DR group). Rats in both dietary groups that did not exhibit a terminal weight loss died at younger ages than those exhibiting the loss. Terminal weight loss in the AL group was not associated with decreased food intake; indeed, half of the rats in this group had an increased food intake during the period of terminal weight loss. This finding is not in accord with the presently held hypothesis. In the DR group, terminal weight loss was associated with reduced food intake. Pathology (renal disease and neoplasms) did not explain the presence or absence of the association between reduced food intake and weight loss in either dietary group. The duration of the period of terminal weight loss was similar for the AL and DR groups. Apparently, restricting calories delays the occurrence but does not affect the duration of senescent terminal weight loss. caloric restriction; food intake; hypothalamic function LOSS OF WEIGHT CULMINATING in death commonly occurs in humans at advanced ages and is a hallmark of a geriatric syndrome termed failure to thrive (11). Although in some individuals the loss in body weight is due to age-associated disease, the cause of this weight loss in many elderly individuals is unknown (28).Most rats that live to old ages also exhibit a terminal loss in body weight (5, 27, 33). Blanton et al. (4) proposed that the Fischer 344 (F344) rat is a good animal model for the study of the physiological basis of senescent terminal weight loss. They found the loss of weight to be associated with a decrease in food intake related to the consumption of shorter and smaller meals, rather than a decreased number of daily meals (5). These investigators hypothesized that senescent terminal weight loss is caused by neurochemical alterations in the hypothalamus resulting in dysregulation of food intake relative to the organism's energy needs (4).Since 1975, our laboratory has carried out life span studies on male F344 rats, and it was our impression that senescent weight loss often was not associated with decreased food intake. In the present study we have investigated this issue in three groups of rats studied in the 1980s and early 1990s for which detailed data are available on body weight, food intake throughout the life span, and pathological lesions at t...

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“…Both food restriction and adiposity have been demonstrated to affect longevity in rodents. [43][44][45] All of the animals monitored for lifespan duration in our study were allowed to eat ad libitum, therefore, we suggest adiposity had a greater influence in longevity difference over that of food intake. Although our fat-pad analyses were performed at P60, the Adiposity reduction by Kv1.3 deletion K Tucker et al further acceleration and then plateau in body weight measured during the first 10 months of age, would suggest that the relative comparison in adiposity across the genotypes would persist throughout the lifespan of the animal.…”

Section: Discussionmentioning

confidence: 95%

Kv1.3 gene-targeted deletion alters longevity and reduces adiposity by increasing locomotion and metabolism in melanocortin-4 receptor-null mice

2008

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Objective: Gene-targeted deletion of the voltage-gated potassium channel, Kv1.3, results in 'super-smeller' mice that have altered firing patterns of mitral cells in the olfactory bulb, modified axonal targeting to glomerular synaptic units, and behaviorally have an increased ability to detect and discriminate odors. Moreover, the Kv1.3-null mice weighed less than their wild-type counterparts, have modified ingestive behaviors, and are resistant to fat deposition following a moderately high-fat dietary regime. In this study, we investigate whether or not gene-targeted deletion of Kv1.3 (Shaker family member) can abrogate weight gain in a genetic model of obesity, the melanocortin-4 receptor-null mouse (MC4R-null). Design: Mice with double gene-targeted deletions of Kv1.3 and MC4R were generated by interbreeding Kv1.3 (Kv)-and MC4R-null mouse lines to homozygosity. Developmental weights, nose to anus length, fat pad weight, fasting serum chemistry, oxygen consumption, carbon dioxide respiration, locomotor activity and caloric intake were monitored in control, Kv-null, MC4R-null and Kv/MC4R-null mice. Physiological and metabolic profiles were acquired at postnatal day 60 (P60) in order to explore changes linked to body weight at the reported onset of obesity in the MC4R-null model. Results: Gene-targeted deletion of Kv1.3 in MC4R-null mice reduces body weight by decreasing fat deposition and subsequent fasting leptin levels, without changing the overall growth, fasting blood glucose or serum insulin. Gene-targeted deletion of Kv1.3 in MC4R-null mice significantly extended lifespan and increased reproductive success. Basal or light-phase mass-specific metabolic rate and locomotor activity were not affected by genetic deletion of Kv1.3 in MC4R-null mice but darkphase locomotor activity and mass-specific metabolism were significantly increased resulting in increased total energy expenditure. Conclusions: Gene-targeted deletion of Kv1.3 can reduce adiposity and total body weight in a genetic model of obesity by increasing both locomotor activity and mass-specific metabolism.

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Changes in Adipose Mass and Cellularity Through the Adult Life of Rats Fed Ad Libitum or a Life-Prolonging Restricted Diet

Cited by 192 publications

References 0 publications

Long-term effect of energy restriction at different protein levels on several parameters of nutritional assessment.

Long-term effect of energy restriction at different protein levels on several parameters of nutritional assessment.

Senescent terminal weight loss in the male F344 rat

Kv1.3 gene-targeted deletion alters longevity and reduces adiposity by increasing locomotion and metabolism in melanocortin-4 receptor-null mice

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