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Results for “Caloric Restriction”

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PubMed1997

Relationship between training frequency and subcutaneous and visceral fat in women.

We examined the interaction of two different frequencies of aerobic exercise training (30 min at 50-60% of maximal heart rate reserve per session) and a self-administered caloric restriction program on the changes in subcutaneous (SFM) and visceral (VFM) fat mass over a period of 13 wk. Twenty-six sedentary young women (27.9% body fat) were randomized into three groups: nonexercising control (C, N = 8); 1-2 sessions/wk plus a 240 kcal caloric restriction (1-2SW, N = 9); and 3-4 sessions/wk without caloric restriction (3-4SW, N = 9). There was a equivalent decrease in the percentage of body fat and total fat mass in both exercise groups compared with that in C. Reduction in SFM was significant in 3-4SW, but not in 1-2SW or C. A negative correlation was observed between training frequency and changes in SFM (r = -0.65). In contrast, VFM decreased significantly and equivalently in both 1-2SW and 3-4SW, but there was no correlation between training frequency and changes in VFM (r = 0.20). It is suggested that the decrease in SFM, but not VFM, is proportional to the amount of aerobic exercise training. A change in VFM appears to be related to an deficit in caloric balance either by dietary restriction (decrease caloric intake) or by increased caloric expenditure.

Abdomen↗

PubMed1988

Effects of weight loss on clinic and ambulatory blood pressure in normotensive men.

Obesity and physical inactivity are associated with both elevated cardiovascular risk and blood pressure (BP), but the interrelation of exercise, weight loss and BP is poorly understood. This study examines the independent effects of exercise and weight loss on both standard clinic and automated, ambulatory BP in 115 overweight, sedentary, normotensive men (aged 30 to 59 years) who were randomly assigned to control status or to lose weight over 1 year by moderate caloric restriction (dieting) or by increased caloric expenditure (exercise). Median daytime and evening BP were determined from measurements made every 20 minutes while the subjects were awake. After 1 year, the control group gained (mean +/- standard deviation) 0.5 +/- 3.8 kg while the diet group lost 6.9 +/- 4.4 kg and the exercise group lost 4.6 +/- 3.5 kg. Clinic BP decreased similarly in all 3 groups, but daytime and evening ambulatory BP decreased in both intervention groups and increased in the control group. Relative to the 1-year change in control subjects, net change in daytime ambulatory BP averaged -2 to -3 mm Hg in both dieters and exercisers, while net change in evening ambulatory BP averaged -3 to -4 mm Hg. These changes were all statistically significant (p less than 0.05) when compared with control subjects except for daytime systolic BP in both intervention groups and evening diastolic BP in dieters. Weight loss achieved through caloric restriction or expenditure may cause important decreases in BP in normotensive men; exercise appears to confer no unique benefit. If confirmed, these results have important public health implications for the prevention of cardiovascular disease.

Adult↗

PubMed1988

Blood pressure in obese adolescents: effect of weight loss.

The BP distribution of a group of 72 obese adolescents was determined both before and after weight loss. Weight loss was produced by a program of caloric restriction and behavior change alone (n = 26) or with a combination of caloric restriction, behavior change, and exercise (n = 25). It was demonstrated that obese adolescents have a BP distribution that is skewed 1 SD to the right of normal (P less than .01), and that with weight loss this distribution was no longer different from that of the general population. It was also shown that a weight loss program that incorporates exercise and caloric restriction produces the most desirable effect on BP reduction (ie, greatest decrease in resting systolic BP and greatest decrease in exercise diastolic and mean BP). Finally, it was demonstrated that obese adolescents have structural changes present in the forearm resistance vessels and that these structural changes are reversed to the greatest extent in the weight loss program that includes exercise.

Adolescent↗

PubMed2026

Tissue origins of the plasma proteomic response to glucose ingestion in humans.

AIMS/HYPOTHESIS: Circulating proteins act as important hormonal signals of nutrient intake. We aimed to systematically characterise the time-resolved proteomic response to glucose ingestion in humans, and to assess its robustness following prolonged complete caloric restriction. METHODS: We conducted oral glucose tolerance tests (OGTTs) in 11 healthy volunteers before and after 7 days of complete caloric restriction and measured the response of >2900 targets through high-resolution plasma protein profiling. RESULTS: We identified a signature of 44 proteins that changed significantly following glucose ingestion, which was reproducible after 7 days without food, and was strongly (20-fold) enriched for 'stomach-specific' proteins. We report that annexin A10 (ANXA10) shows the most significant post-glucose change observed, similar to the trajectories of secreted hormones. We present observational human evidence from multiple sources suggesting that ANXA10 is secreted upon sensing an increase in gastric pH, with the stomach as the major contributing tissue. Despite a profound metabolic shift after 7 days of complete caloric restriction, characterised by delayed insulin secretion and postprandial hyperglycaemia, only four proteins showed robust evidence for a differential trajectory during both OGTTs. This included plasma levels of tryptophanyl-tRNA synthetase 1 (WARS), for which we found a genetic association with glucose homeostasis and coronary artery disease. CONCLUSIONS/INTERPRETATION: Our exploratory study identifies the proteomic response to glucose ingestion and demonstrates its reproducibility despite major shifts in glucose homeostasis. We characterise the gastrointestinal origin of these changes, and hypothesise a hitherto under-recognised role for sensing of changes in gastric pH on the plasma proteome.

Humans↗

PubMed1986

Influence of caloric intake on experimental carcinogenesis: a review.

The effect of caloric intake on tumor growth has been recognized for over 70 years. Inhibition of tumor growth depends primarily on the extent of caloric restriction, but tumor type, animal strain, and dietary composition all exert some influence. Caloric restriction is most effective when maintained during both initiation and promotion, but if limited to one of these phases, restriction during promotion appears to be the more effective modality. The types of tumor that have been studied include spontaneous mammary and lung tumors as well as tumors induced by organ-specific carcinogens or irradiation with ultraviolet light. Numerous investigators have studied the effects of fat, and a diet low in calories but high in fat is generally significantly more effective in inhibiting carcinogenesis than is a diet high in calories but low in fat. Mice fed high fat, low calorie diets exhibited 48% fewer chemically induced skin tumors and 61% fewer tumors induced by ultraviolet irradiation than did mice fed low fat, high calorie diets. Mice fed a diet containing 2% fat exhibited a 66% incidence of skin tumors, whereas mice fed an isocaloric diet containing 61% fat showed a 78% incidence. Rats whose diet was restricted in calories by 40% exhibited no mammary tumors (coconut oil as primary dietary fat) or 75% fewer tumors (corn oil as dietary fat) compared to ad libitum-fed controls; they also exhibited 47% fewer colonic tumors. The mechanism by which caloric restriction exerts its tumor-inhibiting effects remains to be elucidated.

Animals↗

PubMed2003

Chronic exercise lowers the defended body weight gain and adiposity in diet-induced obese rats.

The effects of running wheel exercise and caloric restriction on the regulation of body weight, adiposity, and hypothalamic neuropeptide expression were compared in diet-induced obese male rats over 6 wk. Compared with sedentary controls, exercising rats had reduced body weight gain (24%), visceral (4 fat pads; 36%) and carcass (leptin; 35%) adiposity but not insulin levels. Hypothalamic arcuate nucleus (ARC) proopiomelanocortin (POMC) mRNA expression was 25% lower, but ARC neuropeptide Y (NPY), agouti- related peptide, dorsomedial nucleus (DMN) NPY, and paraventricular nucleus (PVN) corticotropin- releasing hormone (CRH) expression was comparable to controls. Sedentary rats calorically restricted to 85% of control body weight reduced their visceral adiposity (24%), leptin (64%), and insulin (21%) levels. ARC NPY (23%) and DMN NPY (60%) were increased, while ARC POMC (40%) and PVN CRH (14%) were decreased. Calorically restricted exercising rats an half as much as ad libitum-fed exercising rats and had less visceral obesity than comparably restricted sedentary rats. When sedentary restricted rats were refed after 4 wk, they increased intake and regained the weight gain and adiposity of sedentary controls. While refed exercising rats and sedentary rats ate comparable amounts, refed exercising rats regained weight and adiposity only to the level of ad libitum-fed exercising rats. Thus exercise lowers the defended level of weight gain and adiposity without a compensatory increase in intake and with a very different profile of hypothalamic neuropeptide expression from calorically restricted rats. This may be due to exercise-related factors other than plasma insulin and leptin.

Adipose Tissue↗

PubMed2003

Role of dietary calcium and dairy products in modulating adiposity.

Dietary calcium plays a pivotal role in the regulation of energy metabolism. High-calcium diets attenuate adipocyte lipid accretion and weight gain during overconsumption of an energy-dense diet and increase lipolysis and preserve thermogenesis during caloric restriction, thereby markedly accelerating weight loss. Our studies of the agouti gene demonstrate a key role for intracellular Ca2+ in regulating adipocyte lipid metabolism and TG storage. Increased intracellular Ca2+ resulting in stimulation of lipogenic gene expression, and lipogenesis and suppression of lipolysis resulting in adipocyte lipid filling and increased adiposity. Moreover, we recently demonstrated that the increased calcitriol produced in response to low-calcium diets stimulates adipocyte Ca2+ influx and, consequently, promotes adiposity. Accordingly, suppressing calcitriol levels by increasing dietary calcium is an attractive target for obesity intervention. In support of this concept, transgenic mice expressing the agouti gene specifically in adipocytes (a human-like pattern) respond to low-calcium diets with accelerated weight gain and fat accretion, whereas high-calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis, and suppress fat accretion and weight gain in animals maintained at identical caloric intakes. Further, low-calcium diets impede body fat loss, whereas high-calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction. Dairy sources of calcium exert markedly greater effects in attenuating weight and fat gain and accelerating fat loss. This augmented effect of dairy products is likely due to additional bioactive compounds in dairy that act synergistically with calcium to attenuate adiposity. These concepts are confirmed by both epidemiological and clinical data, which demonstrate that increasing dietary calcium results in significant reductions in adipose tissue mass in obese humans in the absence of caloric restriction and markedly accelerates the weight and body fat loss secondary to caloric restriction, whereas dairy products exert significantly greater effects. These data indicate an important role for dairy products in both the prevention and treatment of obesity.

Adipose Tissue↗

PubMed1993

Age-related gliosis in the white matter of mice.

A histopathologic study of the brains from 96 mice, ranging in age from 3 to 57 months in age, documents an age-associated increase in hypertrophic astrocytes in white matter. This report of gliosis is distinct from previously reported proliferation of glial cells in the grey matter. Four genotypes, CBA/HT6J, C57BL/6J, B6CBAT6F1J, and B6C3F1 were positive for this age-related lesion. Most very old mice utilized in this study were calorically restricted, a dietary manipulation long known to result in increased longevity in rodents. Caloric restriction appears to delay the age associated increase of this lesion. Immunoperoxidase staining for the astrocyte-specific glial fibrillary acidic protein (GFAP) confirmed the progressive increase in the density of stainable astrocytes with increase in age. GFAP staining of white matter increased in both diet groups with age. These findings present an interesting model for the study of aberrant cellular activity and perhaps neurodegeneration, modulated by caloric restriction.

Aging↗

PubMed2004

Development of calorie restriction mimetics as a prolongevity strategy.

By applying calorie restriction (CR) at 30-50% below ad libitum levels, studies in numerous species have reported increased life span, reduced incidence and delayed onset of age-related diseases, improved stress resistance, and decelerated functional decline. Whether this nutritional intervention is relevant to human aging remains to be determined; however, evidence emerging from CR studies in nonhuman primates suggests that response to CR in primates parallels that observed in rodents. To evaluate CR effects in humans, clinical trials have been initiated. Even if evidence could substantiate CR as an effective antiaging strategy for humans, application of this intervention would be problematic due to the degree and length of restriction required. To meet this challenge for potential application of CR, new research to create "caloric restriction mimetics" has emerged. This strategy focuses on identifying compounds that mimic CR effects by targeting metabolic and stress response pathways affected by CR, but without actually restricting caloric intake. Microarray studies show that gene expression profiles of key enzymes in glucose (energy) handling pathways are modified by CR. Drugs that inhibit glycolysis (2-deoxyglucose) or enhance insulin action (metformin) are being assessed as CR mimetics. Promising results have emerged from initial studies regarding physiological responses indicative of CR (reduced body temperature and plasma insulin) as well as protection against neurotoxicity, enhanced dopamine action, and upregulated brain-derived neurotrophic factor. Further life span analyses in addition to expanded toxicity studies must be completed to assess the potential of any CR mimetic, but this strategy now appears to offer a very promising and expanding research field.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2006

Aging in mouse and human systems: a comparative study.

This article discusses the significance of mouse models as a basis for elucidating the aging process in humans. We identify certain parallels between mouse and human systems and review the theoretical and empirical support for the claim that the large divergence in the rate of aging between the two species resides in differences in the stability of their metabolic networks. We will show that these differences in metabolic stability have their origin in the different ecological constraints the species experience during their evolutionary history. We exploit these ideas to compare the effect of caloric restriction on murine and human systems. The studies predict that the large increases in mean life span and maximum life-span potential observed in laboratory rodents subject to caloric restriction will not obtain in human populations. We predict that, in view of the different metabolic stability of the two systems, caloric restriction will have no effect on the maximum life-span potential of humans, and a relatively minor effect on the mean life span of nonobese populations. This article thus points to certain intrinsic limitations in the use of mouse models in elucidating the aging process in humans. We furthermore contend the view that these limitations can be mitigated by considering the metabolic stability of the two species.

Aging↗

PubMed2004

Lack of correlation between mitochondrial reactive oxygen species production and life span in Drosophila.

The free radical theory of aging proposes that mitochondrial production of reactive oxygen species (ROS) determines the rate of aging. Supporting this hypothesis, longer-lived species produce fewer ROS than shorter-lived ones, and calorically restricted rodents live longer and produce fewer ROS than controls. We studied such correlation in Drosophila melanogaster in caloric restriction and in mutant flies overexpressing the mitochondrial adenine nucleotide translocase (ANT). Caloric restriction extended life span, but there was no significant difference in mitochondrial ROS production compared with controls. ANT overexpressers had significantly lower ROS production (because they had lower membrane potential), but their life span was not extended compared to wild type. Our results show two examples in which mitochondrial ROS production and life span are not correlated.

Aging↗

PubMed2005

Aging: gene silencing or gene activation?

According to the author's theory of gene silencing, the key process in aging involves reduced expression of a number of genes. Silencing of genes has a complex mechanism, which involves methylation of DNA, histone modification and chromatin remodeling. In addition to deacetylation of the histones and methylation of DNA, recently described RNAi mechanism could initiate formation of silenced chromatin. Hypermethylation of the promoter will silence the gene. Genome-wide hypomethylation will induce genomic instability, amplification of oncogenes and also silencing of the genes through RNAi mechanism. Studies by different groups, conducted in yeast, worms, flies and mice, confirmed substantial changes in gene expression in aging. Among them, the most important was silencing of tumor suppressors and other genes involved in the control of cell cycle, apoptosis, detoxification, and cholesterol metabolism. There was also increased expression of the smaller group of oncogenes and other genes which are associated with typical diseases of old age. Caloric restriction normalizes expression of a substantial percentage of these genes. Animal studies confirmed importance of caloric restriction, which decreases signaling through the IGF-1/AKT pathway and expression of gene p53. These studies, however, cannot be directly applied to human aging. It is proposed that age management therapy should attempt to normalize gene expression in the older population to the level typical for young adults. This would require activation of silenced genes and normalization of overexpressed genes. Caloric restriction and exercise are helpful in decreasing the activity of important oncogenes and activation of silenced tumor suppressors, and may have a positive impact, not only on aging, but also on prevention of cancer. Dietary supplements containing phytochemicals should normalize increased expression of oncogenes. Examples are: genistein and EGCG, which effect signaling through the IGF-1/AKT pathway and resveratrol and limonen, which do so through the RAS pathway. A group of amino acid derivatives and organic acids of animal and human origin should activate silenced tumor suppressor genes (Aminocare A10, Aminocare Extra). Among them 3-phenylacetylamino-2, 6-piperidinedione intercalates specifically with DNA and protects sequences of tumor suppressor genes, which are vulnerable to the effects of carcinogens. Phenylacetate activates p53 and p21 through inhibition of methyltransferase and farnesylation of the RAS protein. Phenylbutyrate activates tumor suppressor genes through inhibition of histone deacetylation. Phenylacetylglutamine decreases genomic instability and expression of oncogenes and promotes apoptosis. The application of DNA microarray techniques to human studies should provide more information about differences in gene expression in different age groups and help design more effective age management regimens.

Adaptation, Physiological↗

PubMed2004

Calorie restricted diet and urinary pentosidine in patients with rheumatoid arthritis.

Low-energy diets and fasting have suppressive effects on rheumatoid arthritis. It was reported recently that urine levels of pentosidine (i.e., an advanced glycation end product formed by glycosylation) is associated with the activity of rheumatoid arthritis. We conducted a regimen of caloric restriction combined with fasting in patients with rheumatoid arthritis, and then evaluated urinary pentosidine levels. Ten patients with rheumatoid arthritis underwent a 54-day caloric restriction program. Urinary pentosidine levels were measured and the Lansbury Index were determined by examining the clinical features, blood biochemistry and the inflammation activity of rheumatoid arthritis on days 0, 25 and 54. On day 0, the mean urinary pentosidine level of patients with rheumatoid arthritis was significantly higher than that of the control subjects. On day 54, the mean body weight had reduced due to caloric restriction. The mean values of the erythrocyte sedimentation rate and the Lansbury Index of patients both significantly decreased during the study. In addition, although the urinary pentosidine levels showed no significant difference between day 0 and 25, it was significantly decreased at the end of the study (day 54). The study showed that under a low energy diet a reduction of disease activity in rheumatoid arthritis was accompanied with a reduction of the urinary pentosidine.

Arginine↗

PubMed1988

Exercise regulation of triiodothyronine metabolism.

Negative caloric balance reduces triiodothyronine (T3) production in both humans and rodents. The effects of chronic voluntary exercise and various levels of caloric intake and balance on T3 metabolism were studied in adult male C57/BL6 mice to determine if exercise had any direct effects on T3 production in vivo and in vitro. Chronic voluntary exercise was induced by the addition of running wheels to cages for 28 days. Ad libitum-fed exercising mice ingested 20% greater calories (P less than 0.02), maintained body weight, and increased T3 production (53.1 +/- 5.3 vs. 42.3 +/- 3.4 ng.h-1.100 mg body wt-1; P less than 0.01). Exercising animals pair fed to sedentary ad libitum-fed controls decreased their body mass to an equivalent degree as underfed sedentary animals (caloric intake 75% of ad libitum-fed controls) but had increased T3 clearance compared with weight-matched underfed sedentary control (P less than 0.05). Animals that were underfed and exercised decreased their body weight to a greater extent (P less than 0.01) compared with the sedentary underfed group, but T3 production rates were equal. Activity of liver 5'-deiodinase activity was decreased almost 50% (P less than 0.01) during both exercise plus pair feeding and exercise plus caloric restriction but decreased only 28% during caloric restriction alone (P less than 0.01). T3 metabolic clearance and production rates in vivo were correlated to caloric intake (r = 0.73, P less than 0.01), but an interaction between exercise and caloric balance was observed. Chronic voluntary exercise modulates T3 metabolism via several mechanisms. Exercise has an apparent stimulatory effect independent of caloric intake, but also there are regulatory effects dependent on the absolute level of caloric intake and relative caloric balance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Why dietary restriction substantially increases longevity in animal models but won't in humans.

Caloric restriction (CR) extends maximum longevity and slows aging in mice, rats, and numerous non-mammalian taxa. The apparent generality of the longevity-increasing effects of CR has prompted speculation that similar results could be obtained in humans. Longevity, however, is not a trait that exists in a vacuum; it evolves as part of a life history and the physiological mechanisms that determine longevity are undoubtedly complex. Longevity is intertwined with reproduction and there is a cost to reproduction. The impact of this cost on longevity can be age-independent or age-dependent. Given the complexity of the physiology underlying reproductive costs and other mechanisms affecting life history, it is difficult to construct a simple model for the relationship between the particulars of the physiology involved and patterns of mortality. Consequently, we develop a hypothesis-neutral model describing the relationship between diet and longevity. Applying this general model to the special case of human longevity and diet indicates that the benefits of caloric restriction in humans would be quantitatively small.

Age Factors↗

PubMed1983

Differential effects of dietary caloric and protein restriction in the aging rat.

Numerous studies have shown caloric restriction retards the physiological decline and increases the life span of animals. However, in these studies protein consumption was also reduced; thus, whether the beneficial effects were due to caloric or to protein restriction is unclear. To examine independently the effects of caloric and protein restriction on growth, renal function, and survival, caloric restricted male rats were fed 18, 30 or 42 percent casein diets that provided two-thirds of the quantity of diet consumed by groups fed 12, 20, or 28 percent casein diets ad libitum, respectively. Hence, caloric restricted groups consumed the same amount of protein as their paired ad libitum fed groups but one-third fewer calories. The results showed that caloric restriction decreased mature body weight, increased the rate of attaining mature body weight, retarded the age-associated decline in renal function, and increased survival. Protein restriction had no effect on mature body weight, decreased maturation rate, improved renal function, and decreased survival. Thus, protein restriction did not contribute to the survival-promoting effects of caloric restriction in rats.

Aging↗

PubMed2006

Fasting leptin and appetite responses induced by a 4-day 65%-energy-restricted diet.

OBJECTIVE: Animal studies show that the leptin decline after acute severe caloric restriction is a peripheral signal to increase food intake. However, most human studies have failed to observe such a relationship. We studied the acute effects of severe caloric restriction on the association between serum leptin concentrations and subjective appetite. SUBJECTS: A total of 44 healthy adult men (aged: 43 +/- 5 years; BMI: 27.3 +/- 3.2 kg/m(2)). MEASUREMENTS: Fasting serum leptin concentrations and self-perceived appetite levels were measured during a 4-day diet containing 36% of the estimated energy requirements. Appetite levels were assessed with a 10-point Likert scale, reflecting hunger, fullness, desire to eat, prospective consumption and total appetite. RESULTS: After the 4-day energy deficit, fasting leptin concentrations decreased by 39.4% (95% CI: -43.6; -34.9%). This decline was associated with an increase in fasting hunger (r = -0.42; P < 0.01), desire to eat (r = -0.39; P < 0.05) and total appetite (r = -0.38; P < 0.05). Furthermore, the association between fasting leptin concentrations and fasting appetite levels became stronger during the energy restriction period (for total appetite: day 0 r = -0.15, P = 0.32; day 2 r = -0.31, P =< 0.05; day 4 r = -0.41, P < 0.01). CONCLUSIONS: The acute proportional reduction in fasting leptin after 4-day energy restriction is associated with an increase in self-perceived appetite. Additionally, the inverse association between proportional fasting leptin concentrations and self-perceived appetite response becomes stronger as energy restriction is prolonged. These findings suggest that leptin has an instrumental role in restoring energy balance in humans through the expression of appetite.

Adult↗

PubMed1995

Use of very-low-calorie diets in the treatment of obese persons with non-insulin-dependent diabetes mellitus.

This article discusses the use of very-low-calorie diets (VLCDs) in the treatment of obese persons with non-insulin-dependent diabetes mellitus (NIDDM). Research using VLCDs with overweight participants with and without diabetes is reviewed. In both groups of participants, it has been shown that VLCDs used in combination with behavior therapy increase initial weight loss. However, to date, it has not been possible to develop treatment programs that maintain this weight loss long term. Neither intensive maintenance sessions nor intermittent VLCDs have been successful in maintaining the benefits of VLCDs long term. Thus, from the perspective of producing long-term weight loss, balanced low-calorie diets appear to be as effective as VLCDs. However, VLCDs may be useful in treating obese persons with NIDDM, because caloric restriction independent of notable weight loss has marked effects on glycemic control. Several studies have shown that just 7 days of caloric restriction can produce dramatic improvements in glycemic control; moreover, VLCDs produce greater improvements in glycemic control than more moderate diets, even if weight losses are the same. Research is needed to explore new ways to use VLCDs and other approaches to caloric restriction in the treatment of obese persons with NIDDM.

Blood Glucose↗