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Results for “Caloric Restriction”

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PubMed2000

Hypophosphatemia secondary to oral refeeding in anorexia nervosa.

OBJECTIVE: Hypophosphatemia is a well-known complication of the refeeding syndrome in severe cases of anorexia nervosa, described mostly as a result of refeeding with total parenteral nutrition. Few cases have been reported secondary to either nasogastric or oral refeeding. METHOD: The authors present three cases in which hypophosphatemia developed secondary to oral refeeding in severe anorexia nervosa. RESULTS: All 3 patients developed significant hypophosphatemia, to a low of 0.9 mg/dl in two cases and a low of 1. 7 mg/dl in the third. The first patient received close to 3,000 calories per day, along with intravenous fluids, in the hospital; the other 2 patients ate large amounts for several days at home. Caloric restriction and replenishment with phosphorous resulted in a rapid return of phosphorous values to normal levels. DISCUSSION: Those who treat severely malnourished patients with eating disorders, whether as inpatients or outpatients, need to be vigilant for the development of the refeeding syndrome, even in patients receiving oral refeeding alone.

Adolescent↗

PubMed1997

Aging and the brain: a new frontier.

With aging, both "normal" senescent age-related changes (ARCs) and late-onset diseases affect the brain, producing declines in performance. The brain as a postmitotic structure is particularly vulnerable to ARCs, and senescence is by far the most powerful risk factor for neurological diseases of the elderly such as sporadic Alzheimer's disease. The concept of senescence as an immutable result of the passage of time is yielding to understanding of the biology of ARCs. Both individual and species differences in longevity illustrate the variable effects of time. Whereas human life expectancy has been extended by prevention and treatment of specific diseases, life span can be altered by modifying the processes producing ARCs. Models of prolonged life span (eg, modifications of Caenorhabditis elegans longevity genes, restricted caloric intake) demonstrate the feasibility of extending longevity throughout the phylogenetic spectrum. Both programmed and variable factors produce ARCs. Cell survival depends on a balance of opposing factors--oncogene and anti-oncogene products, cyclins, growth factors, and so on; apoptotic death results when the balance shifts. Variable factors, including accumulation of oxygen free radicals, protein conformational changes, decline in chaperone functions, and secondary loss of mitochondrial energy production, can also result in neuronal degeneration. To prevent the increased neuronal vulnerability of senescence, ARCs must be modified. The "new frontier" in neurology is the challenge of understanding the changes of aging, both to determine their impact on disease and to prevent their consequences.

Aging↗

PubMed2002

Quiet please, do not disturb: a hypothesis of embryo metabolism and viability.

This review uses nutritional markers of normal and impaired development to address the question; what makes a viable mammalian preimplantation embryo? Resolution of this question is important to ensure the long-term safety of embryo-based biotechnologies in man and domestic animals, the optimisation of embryo production and culture conditions and the development of methods to select viable embryos for replacement. After considering the nutrition of embryos and somatic cells, and the phenomenon of caloric restriction, it is concluded that preimplantation embryo survival is best served by a relatively low level of metabolism; a situation achieved by reducing the concentrations of nutrients in culture media and encouraging the use endogenous resources.

Animals↗

PubMed2003

The role of palatable food and hunger as trigger factors in an animal model of stress induced binge eating.

OBJECTIVE: Dieting and stress are etiological factors in eating disorders, and dieting strongly predicts stress-induced overeating in the nonclinical population. We developed an animal model of binge eating in sated rats that is evoked by stress, but only in rats with a history of caloric restriction and only if highly palatable food (HPF) is available after stress. This study investigated the effect of known binge triggers, a taste of HPF and of hunger, on this type of binge eating. METHOD: Female rats were cycled through the R/S protocol but this time were given just a taste of HPF with ad lib regular chow. After another R/S cycle, rats were stressed during restriction (while hungry) and were given HPF and chow. RESULTS: Although binge eating did not occur if only chow was available after stress, just a taste of HPF sufficed to increase chow intake to more than 160% (p < 0.001) of rats with a history of restriction only, stress-only, or neither. Hunger increased the proportion of chow consumed by both restricted groups, but stress magnified this hunger-induced overeating by increasing HPF intake to 137% of restriction-only rats (p < 0.001). DISCUSSION: These effects suggest that binge eating in this model is motivated by reward, not metabolic need, and parallels observations of binge triggers described in clinical binge-eating disorders. This strengthens the validity of using this animal model to target the physiology and treatment of eating disorders preceded by dieting and stress.

Animals↗

PubMed2007

A history of human-like dieting alters serotonergic control of feeding and neurochemical balance in a rat model of binge-eating.

OBJECTIVE: This study replicated a model of stress-induced binge-eating in rats with a history of caloric restriction (HCR), tested their response to SSRI (fluoxetine) treatment, and explored changes in brain monoamine levels. METHOD: Young female rats with no-HCR/no-Stress, no-HCR/Stress, HCR/no-Stress, and HCR+Stress (binge-eating) were treated with fluoxetine. Post-mortem levels of serotonin, dopamine, and metabolites were assessed from brain regions key to feeding and reward. RESULTS: A 3 mg/kg dose of fluoxetine without effect in the no-HCR groups suppressed intake of HCR groups, normalizing the binge-eating of HCR/Stress rats. No differences in monoamines were detected in the hypothalamus or tegmentum but a strong positive relationship between accumbens serotonin and dopamine turnover in no-HCR rats was absent in rats with HCR. CONCLUSION: Despite lack of hunger, a history of human-like dieting alters serotonin function in ways suggesting consequences not only to feeding but also control of reward and mood that are dependent on dopamine/serotonin interactions.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1980

The effect of diet on autogenous immunity to mouse mammary tumor virus in C3H/Bi mice.

Antibody levels to mouse mammary tumor virus (MuMTV) in sera of C3H/Bi, C57BL/6 and AKR mice were assayed by an enzyme-linked immunosorbent assay (ELISA). It was found that antibody levels to MuMTV were highest in sera of C3H/Bi females which have a high incidence of breast cancer and low in male C3H/Bi and female C3H/Bi foster-nursed on C57BL/6 females. Sera of C57BL/6 and AKR mice showed very low or undetectable levels of antibody to MuMTV. Reduction of caloric intake sufficient to inhibit mammary tumor formation strikingly inhibited formation of antibody against MuMTV. The lowest levels of antibody were observed in sera of mice fed 10 cal/day of a defined diet. Significantly higher levels developed in the sera of mice fed 16 cal/day of the same defined diet. The highest antibody levels against MuMTV, however, were seen in sera of mice fed lab chow ad libitum but no correlation was evident between levels of antibody and tumor size. These studies indicate that dietary caloric restriction has a profound influence on the development of both mammary adenocarcinoma and antibody responses to MuMTV.

Age Factors↗

PubMed1987

Comparison between the effects of dietary fat level and of calorie intake on methylnitrosourea-induced mammary carcinogenesis in female SD rats.

The aim of this study was to separate the effects of calorie intake on tumorigenesis from those of fat content and fat composition in an animal model. Our principal observations were the following. Decreasing the calorie level by 30% significantly inhibited tumor development in any observed parameter of tumorigenesis, independently of the level of fat. The fat content of semi-synthetic diets, although varying by 44.4%, did not significantly influence mammary tumorigenesis; in fact, carcinogenic expression was discontinuously related to the fat level. A plateau of tumor incidence was observed at the level of 35 energy percentage of fat. Fat composition did not influence tumorigenesis or body weight gain. The role of caloric restriction is thus stressed in relation to possible dietary prevention of cancer.

Animals↗

PubMed2005

Effects of nickel poisoning on expression pattern of the 72/73 and 94 kDa stress proteins in rat organs and in the COS-7, HepG2, and A549 cell lines.

The present study deals with the effects of Ni on the expression level of three stress proteins, namely, the cytosolic HSP72 and HSP73, and the reticulum-associated GRP94. Experiments were carried out on "Wistar'' female rats daily injected with 4 mg NiCl2 per kg body weight for 1, 3, 5, and 10 days. Another set of experiments were carried out using cell lines, derived from the monkey kidney (COS-7), and from human tumors of the lung (A549) and liver (HepG2). Cells were cultured for 4 days in the permanent presence of 100, 200, or 400 microM NiCl2. In control rats, stress proteins pattern was found to be tissue specific: two protein bands of 96 and 94 kDa were immunodetected with the anti-GRP94 antibody in kidney and liver extracts, whereas only the 96 kDa band was present in ovary extracts. HSP73 was present in kidney, liver, and ovary whereas HSP72 was only found in kidney. In kidney of nickel-treated animals, HSP73 and the 96 kDa proteins were overexpressed whereas HSP72 was strongly down regulated. No such effect was observed in liver or ovary. Similarly, in nickel-treated cell lines, HSP72 was downregulated and GRP94 (96 kDa protein) was overexpressed. HSP73 expression appeared moderately increased in A549 cells but decreased in COS-7 cells. Because long-term caloric restriction was reported to reduce free radical generation in cells, the effect of 1 month food restriction (50%) was tested in rats as a possible way to lower oxidative damages induced by Ni. No significant effect on HSP expression was observed.

Animal Feed↗

PubMed2003

Expression of lactate dehydrogenase A and B genes in different tissues of rats adapted to chronic hypobaric hypoxia.

Lactate dehydrogenase (LDH) is a tetramer made up of two different subunits A and B. In cellular models, severe hypoxia increases LDH A gene expression whereas LDH B gene does not exhibit any regulation. The aim of our work was to characterise LDH expression in different tissues of rats bred at high altitude. For this purpose, we chose a Sprague-Dawley rat strain adapted to chronic hypoxia in La Paz (3700 m), Bolivia. Two normoxic control groups were bred at low altitude in Clermont-Ferrand (350 m), France, one group was ad libitum with free access to food and water as was the hypoxic one, and the second normoxic group was nourished with the food intakes measured for the animals from La Paz. We measured total LDH specific activity, isoform distribution and LDH A and B mRNA amounts in three skeletal muscles (soleus, extensor digitorum longus (EDL), plantaris), heart and brain. Our study demonstrates that, unlike what has been shown in cellular models under severe hypoxia, LDH A gene is not systematically up-regulated in tissues of rats living at high altitude. Furthermore, chronic hypoxia limits LDH B gene transcription or its mRNA stability in both soleus and EDL. These regulations occur at various molecular levels like gene transcription, mRNA stabilisation or translation and protein stability, depending on the tissue studied, and are partly attributed to caloric restriction provoked by high altitude. These data provide insight into LDH gene expression underlying the diverse and complex tissue-specific response to chronic hypoxia.

Adaptation, Physiological↗

PubMed2004

Differential expression of transforming growth factor-beta in the interstitial tissue of testis during aging.

Transforming growth factor-betas (TGF-betas) have significant effects on testis development. The pattern of TGF-beta expression in aging testis has not been established to date. We examined age-related changes in the expression of TGF-beta and its receptors in the testis using Western blot analysis. TGF-beta1 expression increased continuously in aging rat testis, whereas no age-associated changes were observed for TGF-beta3. Strong expression of TGF-beta2, as well as type I and II receptors was observed in 12-month-old testis, but following this time, expression decreased dramatically. Interestingly, TGF-beta2 and -beta3 displayed strong and similar expression patterns in liver, regardless of age, suggesting that the down-regulation of TGF-beta2 is testis-specific. We observed significant induction of p53 and p21WAF1 in 18-month-old testis that appeared to correspond with aging. Moreover, caloric restriction (CR) prevented age-related decrease in TGF-beta2 expression. Using immunohistochemistry, we showed that all TGF-beta1, -beta2, and -beta3 proteins are expressed primarily in interstitial cells, which are located in the space between adjoining seminiferous tubules. Our data collectively indicate that aging in the testis is regulated by differential expression of TGF-beta proteins, and decreased levels of TGF-beta2 contribute to the aging process.

Aging↗

PubMed2003

Sonographic assessment of changes in thickness of different abdominal fat layers in response to diet in obese women.

PURPOSE: We evaluated the potential application of sonography to monitor alterations in abdominal fat thickness in obese women before and after dieting. METHODS: This study included 40 obese women (mean age, 42.2 +/- 9.4 years; mean body mass index [BMI], 36.0 +/- 5.9 kg/m2) who underwent a 3-month low-calorie diet. Height, weight, waist circumference (WC), and hip circumference (HC) were measured. BMI and waist-to-hip ratio (WHR) were calculated. Abdominal subcutaneous (S) and intra-abdominal preperitoneal (P) fat were measured at their maximum (max) and minimum (min) thickness sites using a 7.5-MHz linear-array probe. Intra-abdominal visceral (V) fat was measured using a 3.5-MHz convex-array probe. Measurements were taken before and after caloric restriction. RESULTS: The mean weight was reduced from 88.6 +/- 17.1 kg to 83.0 +/- 15.9 kg (p < 0.0001). The mean changes in S(min) (r = 0.376, p = 0.017), S(max) (r = 0.508, (p = 0.001), P(min) (r = 0.439, p = 0.005), and V (r = 0.365, p = 0.022) fat thicknesses were positively correlated with change in weight; the change in P(max) fat thickness showed the best and most significant correlation (r = 0.591, p < 0.0001). BMI (r = 0.969, p < 0.0001), WC (r = 0.510, p = 0.001), and HC (r = 0.422, p = 0.007) changes were also positively correlated with weight change, but the WHR change (r = 0.019, p > 0.05) was not. CONCLUSIONS: All the abdominal fat layers, particularly the intra-abdominal P fat, will decrease in response to loss of body fat by dieting. Sonography seems to be useful in monitoring small variations in the thicknesses of abdominal S and intra-abdominal P and V fat.

Abdomen↗

PubMed1991

Influence of volume expansion on capillary transport in the gut of Pichindé virus infected strain 13 guinea pigs.

Hydropenic strain 13 guinea pigs (GP13) injected with Pichindé virus show marked jejunal capillary disruption determined by a reduction in protein reflection coefficient (sigma) [Katz and Starr, 1990]. These studies examined whether this is reversed by a 2% Ringer's expansion, and whether anorexia may contribute to reduced sigma. GP13 were either infected or given a 60% expected ad lib diet, and were studied while under a 2% Ringer's expansion. The results showed 1) infected GP13 separated into groups with either a persistently low sigma (volume unresponsive) or a normal sigma (volume responsive), but no obvious feature of the animals could predict responsiveness; 2) caloric restriction had minimal to no effect on sigma; and 3) both responsive and unresponsive GP had increased heart, lung, and kidney weights. Volume expansion may have salutary effects in some infected GP13, and this is probably due to pressure mediated effects on the capillary wall. The findings support the possibility that conservative management of hemorrhagic fevers may directly ameliorate capillary leak.

Animals↗

PubMed1994

Towards a network theory of ageing: a model combining the free radical theory and the protein error theory.

Many different theories of ageing have been proposed, based often on highly specific molecular causes. Recent advances in evolutionary theory support the idea that ageing is caused by progressive accumulation of defects, but indicate that multiple processes are likely to operate in parallel. This calls for an understanding of ageing and longevity in terms of a network of maintenance processes that controls the capability of the system to preserve homeostasis. Here we develop a theoretical model which begins the task of implementing a Network Theory of Ageing. To do this the model integrates the ideas of the Free Radical Theory, describing the reactions of free radicals, antioxidants and proteolytic enzymes, with the Protein Error Theory, describing the error propagation loops within the cellular translation machinery. The simulations show that an increased radical production and/or insufficient radical protection can destabilize an otherwise stable translation system. The model supports the idea that caloric restriction prolongs life via a reduction of the generation of radicals. Another result of the model is that protein half-life increases with time as a natural consequence of the interaction between proteolytic enzymes and radicals. Finally the model strengthens certain evolutionary ageing theories by showing that there is a positive correlation between maintenance related energy consumption and lifespan.

Aging↗

PubMed2001

Complex adaptive systems, aging and longevity.

Mortality and reproduction are intimately entwined in the study of aging and longevity. I apply the modern theory of complex adaptive systems (nonlinear, stochastic, dynamic methods) to questions of aging and longevity. I begin by highlighting major questions that must be answered in order to obtain a deeper understanding of aging. These are: (i) What should (in an evolutionary sense) mortality trajectories look like? (ii) Why does caloric restriction slow aging? (iii) Why does reproduction cause delayed mortality? (iv) Why does compensatory growth cause delayed mortality? I show how dynamic state variable models based on stochastic dynamic programming (Clark & Mangel, 2000) can be used to embed genetic theories of senescence (either mutation accumulation or antagonistic pleiotropy) in the somatic environment, as George Williams called for in 1957, and how they make the disposable soma theory of aging operational. Such models will allow unification of genetic and phenotypic theories of aging.

Adaptation, Physiological↗

PubMed1975

Trypanosoma lewisi, Trypanosoma rhodesiense: mitotic activity in normal and folic acid deficient rats.

Ten experiments were performed to compare mitotic activity in livers of rats infected with Trypanosoma rhodesiense and Trypanosoma lewisi. The host dietary groups were: (1) complete of full complement; (2) folic acid deficient, and (3) pair-fed or calorically restricted. Liver mitotic counts of T. lewisi-infected rats fed complete and pair-fed control diets showed a high degree of significance over that of control rats. From days 35 to 55, liver mitotic counts of T. lewisi-infected rats deficient in folic acid showed an average of 16 +/- 2 mitotic phases as compared to 9 +/- 2 for livers of uninfected animals. Liver mitotic counts of T. rhodesiense-infected and non-infected rats fed complete and pair-fed control diets showed that there were essentially no differences in the mitotic counts from that seen in liver from control, uninfected animals. On day 25 (day 5 of infection), folic acid-deficient infected rats showed a significantly higher number of dividing cells than the controls. Folate was measured in isolated, washed T. lewisi and T. rhodesiense cells. T. lewisi and T. rhodesiense contained 9.6 ng folate per 10(8) cells and 6.2 ng of folate per 10(8) cells respectively. Metabolic products of T. lewisi contained an average of 0.51 ng of folate per 10(8) trypanosomes. T. rhodesiense metabolic products contained 0.3 ng of folate per 10(8) trypanosomes.

Animals↗

PubMed1977

Iron metabolism in Trypanosoma lewisi infection: serum iron and serum iron-binding capacity.

Progressive changes in iron levels, total iron binding capacity and hematocrit values in sera of rats infected with Trypanosoma lewisi are described. The host dietary group were: (1) complete or full complement; (2) iron-deficient, and (3) pair-fed or calorically restricted. The hematocrit values of T. lewisi-infected rats given the various diets were not significantly different from those of the controls. The decrease in total iron binding capacity (TIBC) of rats inoculated with T. lewisi and fed complete and pair-fed diets ranged up to 15% over uninfected controls. TIBC levels in rats fed an iron-deficient diet and inoculated with T. lewisi ranged up to 32% over uninfected controls. TIBC levels of deficient infected rats were significantly different from the controls from day 90 to infection to the end of the observation period. Serum iron (SI) values of non-infected rats regardless of dietary regimen showed significantly higher values than T. lewisi-infected animals between days 95 and 120. The average SI value, for this period, in adequately fed control rats was 204 +/- 7 microgram/100 ml as compared to 172 +/- 5 microgram/100 for trypanosome-infected rats. SI levels of rats on a pair-fed diet and infected with T. lewisi decreased to 17% over uninfected controls. SI levels of animals on an iron-deficient diet and infected with T. lewisi decreased up to 76% over uninfected controls.

Animals↗

PubMed1989

Serotonin turnover in rat brain during semistarvation with high-protein and high-carbohydrate diets.

Serotonin (5-HT) and 5-hydroxyindolacetic acid (5-HIAA) were determined in seven brain regions of semistarved and control male rats. After semistarvation on a high carbohydrate diet serotonin turnover, as indicated by 5-HIAA/5-HT ratio, was increased in the total brain and several regions both three and 24 hours after the last meal. In contrast, after semistarvation on a high-protein diet serotonin turnover was decreased three hours after ingestion of the final meal, but increased 24 hours thereafter. Compulsary running wheel activity for one hour did not influence diet induce changes in serotonin turnover. Alterations in plasma corticosterone during semistarvation were not related to changes in central serotonin turnover. Data suggest that the interaction of caloric restriction and diet composition determines serotonin turnover during semi-starvation.

Animals↗

PubMed1989

[Food habits of today's adolescents: epidemiological and psychosocial aspects].

Adolescence is a period of life often characterized by inconsistent, experimental and risky behaviour. The study of alimentary habits of adolescents is of particular importance since these determine whether nutritional needs will be met. Whereas an epidemiologic approach seeks to determine the number, the role, and the weight of the multiple determinants of these behaviours, a psycho-social approach leads to the consideration of factors much more difficult to quantify. This paper is based on a local pilot study covering 161 male and female apprentices 15 to 21 years of age, as well as on data available from the recent literature. First, a review of common behaviours such as skipping meals, snacking between meals, and concerning food preferences and aversions is presented. We then review in greater depth two recent publications. The first concerns the attraction that soft drinks have for young people and its consequences for micronutrient balance. The second illustrates the relationship between self-body image and various adolescent attitudes and habits involving caloric restriction. Overall, it appears that data currently available to epidemiologists and "preventologists" concerning adolescent feeding behaviour would not allow them either to reassure those pessimists or worry those optimists whose opposing views on the subject appeared in publications prior to the 1980s. Indeed, there have been but few longitudinal studies of the kind which could let one confirm which subgroups of adolescents are truly at risk of particular health problems as a result of specific types of feeding behaviour.

Adolescent↗