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PubMed2005

Starvation in humans: evolutionary background and contemporary implications.

Although there is extensive evidence that caloric restriction (CR) extends lifespan in several species the evidence base for humans is weak. We are still at the stage of applying inductive reasoning and of framing hypotheses to be tested. It is known that a genetic background contributes about 25% to the variation in human longevity, but thought unlikely that any genes conferring longer lifespan have been positively selected to do so. It is more likely that any such benefits are unintended consequences arising from other adaptations. If there is an association between CR and longevity in humans it may have been selected by previous exposures to famine. This paper briefly reviews the historical evidence on the extent and frequency of famines in human history. It is concluded that starvation has been one of the major selective pressures on the human genome and has left abundant evidence of adaptive survival traits. Many of these are mediated through effects on reproduction. However, interpretation of the possible links between these energy-sparing mechanisms and any association between CR and ageing is handicapped by an absence of data on the latter and will remain a matter of debate for many years to come.

Aging↗

PubMed2004

The many roles of apoptosis in immunity as modified by aging and nutritional status.

Apoptosis plays a vital role in the elimination of anti-self clones, down regulation of immune responses and the killing of virally infected and malignant cells. There is ample evidence that as we age the immune system not only becomes less potent, but dysregulated which includes apoptotic dependent functions. Reductions in the production of naive T and B-cells, reduced cytolytic killing capacity, accumulation of larger numbers of malignant cells, enhanced inflammatory responses, etc., in the aged suggest that apoptosis is dysregulated. Changes in nutritional status can also alter apoptosis. A short period of zinc deficiency (ZD) in young adult mice greatly accelerated apoptosis among pre-B and pre-T cells by 50% to 300% providing a mechanistic explanation for the lymphopenia and thymic atrophy long associated with this and other nutritional deficiencies. Since apoptosis has been shown to be altered by aging and nutritional status, it seemed important to determine how ZD affected these processes in the aged mouse. It was quickly discovered that the pre-B cells were reduced by 80% in the 28 month aged mouse making further studies problematic. In marked contrast to suboptimal zinc, caloric restriction (CR) which when initiated in younger mice delayed the onset of autoimmunity and immunosenescence. CR appeared to also slow the aging of mitochondria and, thereby, reduced the release of reactive oxygen species that damage cells. Thus, it is probable that CR also helped maintain the integrity of mitochondria and apoptotic processes as mice aged. Though CR is not a very practical nutritional model for humans, the outcome of these studies reinforce the potential value of anti-oxidants in our diets. In contrast to their normal nutritional role some nutrients especially small amounts of free metals can induce apoptosis. There is considerable zinc in neurons. As will be discussed, a number of investigators think that this zinc is released during Alzheimer's, Parkinsons's, or brain injury and accelerates apoptosis in surrounding tissues causing greater damage. Data are discussed that indicate nanomoles of free zinc is, indeed, a potent inducer of apoptosis in a variety of tissues. In sum, there is no doubt that nutritional status as well as individual nutrients can modulate apoptosis and that their impact on cell death may become greater in the aged.

Aged↗

PubMed2006

Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue.

Glycogen synthase kinase-3 (GSK-3) is a ubiquitous kinase implicated in both insulin action and adipogenesis. To determine how these multiple roles may relate to insulin resistance, we studied the regulation of GSK-3 protein expression and phosphorylation in skeletal muscle and isolated adipocytes from nonobese healthy control (HC), obese control (OC), and obese type 2 diabetic (OT2D) subjects. At baseline there were no differences in the GSK-3 protein expression in adipocytes. OC subjects underwent a 6-mo caloric restriction resulting in a 7% decrease in body mass index (BMI) and a 21% improvement in insulin-stimulated whole body glucose disposal rate (GDR). GSK-3alpha and GSK-3beta expression decreased in adipocytes (P < 0.05), whereas GSK-3alpha protein expression increased in skeletal muscle (P < 0.05). OT2D subjects were treated with troglitazone or metformin for 3-4 mo. After troglitazone treatment GDR improved (P < 0.05) despite an increase in BMI (P < 0.05), whereas metformin had no significant effect on GDR. There was no significant change in GSK-3 expression in adipocytes following troglitazone, whereas both GSK-3alpha and -beta were decreased in skeletal muscle (P < 0.05). Metformin treatment had no significant impact on GSK-3 protein expression in either adipocytes or skeletal muscle. Neither treatment influenced GSK-3 serine phosphorylation in skeletal muscle or adipocytes. These results suggest that there is tissue specificity for the regulation of GSK-3 in humans. In skeletal muscle GSK-3 plays a role in control of metabolism and insulin action, whereas the function in adipose tissue is less clear.

Adult↗

PubMed2003

Estimation of segmental muscle volume by bioelectrical impedance spectroscopy.

This study validated bioelectrical impedance spectroscopy (BIS) with Cole-Cole modeled measurements of calf and arm segmental water volume and volume changes during 72 h of simulated microgravity and caloric restriction by using magnetic resonance imaging (MRI) muscle volume as a criterion method. MRI and BIS measurements of calf and upper arm segments were made in 18 healthy men and women [age, 29 +/- 8 (SD) yr; height, 171 +/- 11 cm; mass, 71 +/- 16 kg] before and after the intervention. Muscle volume of arm and leg segments by MRI was on average 15 +/- 10 and 14 +/- 8% lower, respectively, than the estimated total water volume by BIS (P < 0.01), but their correlations were excellent (r = 0.96 and r = 0.93, respectively). MRI- vs. BIS-predicted volume changes were a decrease of 49 +/- 68 vs. 41 +/- 62 ml in the calf and a decrease of 18 +/- 23 vs. 11 +/- 24 ml in the arm, respectively (P > 0.05 for both). BIS detected the extracellular water shifts in the calf resulting from the head-down tilt treatment, but the underfeeding protocol was not of sufficient duration or intensity to produce limb intracellular water changes detectable by BIS. BIS was highly correlated with segmental muscle volume and tracked changes associated with head-down tilt. Further research, however, is needed to determine whether BIS can accurately access separate changes in intracellular and extracellular volume.

Adult↗

PubMed2006

How evolutionary thinking affects people's ideas about aging interventions.

Evolutionary theory has guided the development of antiaging interventions in some conscious and some unconscious ways. It is a standard assumption that the body's health has been optimized by natural selection, and that the most benign and promising medical strategies should support the body's efforts to maintain itself. The very concept of natural healing is a reflection of evolutionary thinking about health. Meanwhile, a developing body of experimental evidence points to the startling hypothesis that aging is a metabolic program, under genetic control we are programmed for death. Evolution has provided that the aging program can be abated in times of stress, e.g., caloric restriction. CR mimetics are already recognized as a promising avenue for antiaging research. Beyond this, there are two ancient mechanisms of programmed death in protists that have survived half a billion years of evolution, and still figure in the aging of vertebrates today. These are apoptosis and replicative senescence via telomere truncation. Most researchers have been wary of modifying these mechanisms because they are known to play a stopgap role in cancer prevention. But intriguing evidence suggests that, despite some counter-carcinogenic function, the net result of both these mechanisms may be to shorten lifespan. Thus, interventions that suppress apoptosis and that preserve telomeres may be promising avenues for life extension research. A third element of the body's self-destruction program co-opts the inflammation response. Epidemiological evidence suggests that NSAIDs including aspirin protect against atherosclerosis, arthritis, and some forms of cancer. It may be that aging engages an autoimmune response that can be modified by drugs acting more narrowly on this same pathway. The existence of an evolutionary program that controls aging from the top down supports a new optimism concerning the types of antiaging interventions that are possible, and the likelihood that simple strategies may have dramatic results without dramatic side-effects.

Aging↗

PubMed2005

What are the effects of maternal and pre-adult environments on ageing in humans, and are there lessons from animal models?

An open issue in research on ageing is the extent to which responses to the environment during development can influence variability in life span in animals, and the health profile of the elderly in human populations. Both affluence and adversity in human societies have profound impacts on survivorship curves, and some of this effect may be traceable to effects in utero or in infancy. The Barker Hypothesis that links caloric restriction in very early life to disruptions of glucose-insulin metabolism in later life has attracted much attention, as well as some controversy, in medical circles. It is only rarely considered by evolutionary biologists working on phenotypic plasticity, or by biogerontologists studying model organisms such as C. elegans or Drosophila. One crucial mechanism by which animals can respond in an adaptive manner to adverse conditions, for example in nutrition or infection, during development is phenotypic plasticity. Here we begin with a discussion of adaptive plasticity in animals before asking what such phenomena may reveal of relevance to rates of ageing in animals, and in humans. We survey the evidence for effects on adult ageing of environmental conditions during development across mammalian and invertebrate model organisms, and ask whether evolutionary conserved mechanisms might be involved. We conclude that the Barker Hypothesis is poorly supported and argue that more work in human populations should be integrated with multi-disciplinary studies of ageing-related phenomena in experimental populations of different model species that are subjected to nutritional challenges or infections during pre-adult development.

Adaptation, Physiological↗

PubMed2005

Extended longevity and insulin signaling in adipose tissue.

Caloric restriction and leanness have been shown to increase longevity in organisms ranging from yeast to mammals. Adipose tissue seems to be a pivotal organ in the aging process and in determination of lifespan. We have recently shown that fat-specific disruption of the insulin receptor gene is sufficient to increase lifespan in FIRKO mice, suggesting that reduced adiposity, even in the presence of normal or increased food intake, can extend lifespan. The model also suggests a special role for the insulin-signaling pathway in adipose tissue in the longevity process. Reduced fat mass has an impact on the duration of life in several other model organisms. In Drosophila, a specific reduction in the fat body through overexpression of forkhead type transcription factor (dFOXO) extends lifespan. Furthermore, sirtuin1 (SIRT1), the mammalian ortholog of the life-extending yeast gene silent information regulator 2 (SIR2), was proposed to be involved in the molecular mechanisms linking lifespan to adipose tissue. In the control of human aging and longevity, one of the striking physiological characteristics identified in centenarians is their greatly increased insulin sensitivity even compared with younger individuals. The effect of reduced adipose tissue mass on lifespan could be due to the prevention of obesity-related metabolic disorders including type 2 diabetes and atherosclerosis.

Adipose Tissue↗

PubMed2003

Short-term CR decreases cardiac mitochondrial oxidant production but increases carbonyl content.

Lifelong caloric restriction (CR) reduces the rate of mitochondrial oxidant production and the accumulation of oxidized proteins and prevents some of the age-associated decline in 20S proteasome activity. However, few studies have investigated how rapidly the beneficial effects of CR take place. We investigated whether 2 mo of CR in 6-mo-old rats would be of sufficient duration to elicit these beneficial changes. Mitochondrial oxidant production was significantly diminished in the CR rats compared with the ad libitum-fed animals. Short-term CR also caused a significant decrease in mitochondrial superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities, but there were no differences in cytosolic SOD and GPX activities, whereas mitochondrial and cytosolic catalase (CAT) activity was increased with CR. However, protein carbonyl content was significantly elevated in both the mitochondrial and cytosolic fractions from CR rats. Of the three major 20S proteasome activities (chymotrypsin-like, trypsin-like, and peptidylglutamyl-peptide hydrolase), the peptidylglutamyl-peptide hydrolase activity was significantly elevated in the CR animals, possibly because of the fact that there were more oxidized proteins to be degraded. Although fewer oxidants were produced in the CR animals, it is possible that the ability to scavenge oxidants was transiently suppressed because of the reduction in mitochondrial antioxidant enzyme activities, which may explain the observed increases in carbonyl content.

Animals↗

PubMed1991

Variables controlling the secretion of insulin-like growth factor binding protein-2 in normal human subjects.

Insulin-like growth factor binding protein-2 (IGFBP-2) is one of a family of IGFBPs that are present in extracellular fluids, and binds both IGF-II and IGF-I with high affinity. These studies were conducted to determine the nutritional and hormonal variables that regulate plasma IGFBP-2 concentrations in humans. The mean plasma IGFBP-2 concentration for 38 normal adult subjects was 150 +/- 61 micrograms/L and was 4.7-fold greater than their mean fasting IGFBP-1 value. Mean IGFBP-2 values in cord sera of 26 normal term infants was 3.8-fold greater than the normal adult mean value. Likewise, the mean value for 44 hypopituitary adults was increased 2-fold compared to normal. There was no suppression of IGFBP-2 values in acromegaly. Normal adult subjects showed minimal fluctuations (less than 2-fold changes) in plasma IGFBP-2 concentrations during a 48-h sampling period. These changes were significantly less than the changes that occurred in plasma IGFBP-1 during the same interval. Plasma IGFBP-2 did not change significantly post prandially or after a glucose infusion. Extreme insulin deficiency, after 9 days of fasting, was associated with a 1.7-fold increase in plasma IGFBP-2. Administration of GH, which is known to cause a major decrease in plasma IGFBP-1 and in IGFBP-2 in hypophysectomized animals, did not result in a change in calorically restricted normal adult subjects, suggesting that a normal caloric intake is required for GH to suppress IGFBP-2. In summary, these results show that plasma IGFBP-2 is regulated differently than IGFBP-1. Acute stimulation of insulin secretion does not suppress IGFBP-2, and there is much less daily fluctuation compared to IGFBP-1. These findings suggest that plasma IGFBP-2 levels are more stable than IGFBP-1, and therefore IGFBP-2 may serve as a larger reservior that is available for IGF transport.

Acromegaly↗

PubMed2003

Calorie restriction of a high-carbohydrate diet elevates the threshold of PTZ-induced seizures to values equal to those seen with a ketogenic diet.

The purpose of this study was to evaluate the contributions of ketonemia, caloric restriction, and carbohydrates to seizure protection in rats fed selected diets. Male Sprague-Dawley rats were fed experimental diets of two basic types, one high in carbohydrates and restricted to 90, 65, or 50% of the normal daily caloric requirement and the other a normal rodent chow diet restricted to 90 or 65% of the daily caloric requirement. After consuming their respective diets for 20 days, animals were subjected to tail-vein infusion of pentylenetetrazole (PTZ) to determine seizure threshold, taken as the dose required to evoke the first clonic reaction. Seizure thresholds were compared to those of rats fed control diets of either normal rodent chow fed ad libitum or a standard high-fat (ketogenic) diet calorie-restricted to 90% of daily caloric requirement, all animals age- and weight-matched at the time of diet onset. All diets were balanced for vitamins and minerals and contained at least 10% protein (by weight). Seizure threshold and ketonemia were elevated in both experimental diets in approximate proportion to the degree of calorie restriction. Animals fed the most severely restricted high-carbohydrate diet (50%) had seizure thresholds equal to those fed the ketogenic diet but had significantly lower ketonemia.

3-Hydroxybutyric Acid↗

PubMed2000

Aging does not contribute to the decline in insulin action on storage of muscle glycogen in rats.

Increase in fat mass (FM) and changes in body composition may account for the age-associated impairment in insulin action on muscle glycogen storage. We wish to examine whether preventing the increase in FM abolishes this defect seen with aging. We studied the novel aging model of F1 hybrids of BN/F344 NIA rats fed ad libitum (AL) at 2 (weighing 259+/-17 g), 8 (459+/-17 g), and 20 (492+/-10 g) mo old. To prevent the age-dependent growth in FM, rats were caloric restricted (CR) at 2 mo by decreasing their daily caloric intake by 45% (weighing 292+/-5 g at 8 mo, 294+/-9 g at 20 mo). As designed, the lean body mass (LBM) and %FM remained unchanged through aging (8 and 20 mo old) in the CR rats and was similar to that of 2-mo-old AL rats. However, 8- and 20-mo-old AL-fed rats had three- to fourfold higher FM than both CR groups. Peripheral insulin action at physiological hyperinsulinemia was determined (by 3 mU x kg(-1). min(-1) insulin clamp). Prevention of fat accretion maintained glucose uptake (R(d); 29+/-2, 29+/-2, and 31+/-4 mg x kg LBM(-1) x min(-1)) and glycogen synthesis rates (GS, 12+/-1, 12 +/-1, and 14+/-2 mg x kg LBM(-1) x min(-1)) at youthful levels (2 mo AL) in 8- and 20-mo-old CR rats, respectively. These levels were significantly increased (P<0.001) compared with AL rats with higher %FM (R(d), 22+/-1 and 22+/-2 and GS, 7+/-1 and 8+/-2 mg x kg LBM(-1). min(-1) in 8- and 20-mo-old rats, respectively). The increase in whole body GS in age-matched CR rats was accompanied by approximately 40% increased accumulation of [(3)H] glucose into glycogen and a similar increase in insulin-induced muscle glycogen content. Furthermore, the activation of glycogen synthase increased, i.e., approximately 50% decrease in the Michaelis constant, in both CR groups (P<0.01). We conclude that chronic CR designed to prevent an increase in storage of energy in fat maintained peripheral insulin action at youthful levels, and aging per se does not result in a defect on the pathway of glycogen storage in skeletal muscle.

Aging↗

PubMed1989

Calorie-restricted low-fat diet and exercise in obese women.

The effects of caloric restriction and exercise on body composition, resting metabolic rate (RMR), and maximal oxygen uptake (VO2 max) were studied for 16 wk in 26 premenopausal obese women. Exercise (X) vs nonexercise (NX) was crossed with a low-fat, ad libitum-carbohydrate (AL) diet vs a restricted (R) (800 kcal) low-fat, high-carbohydrate diet in a 2 x 2 factorial design. Subjects were randomly assigned to one of the four treatment groups. Body-weight and percent-fat losses were significant (p less than 0.05) in all groups but greater in subjects assigned to the R diet (p less than 0.05) and/or X (p less than 0.10) groups. Exercise increased (p less than 0.01) VO2 max but neither exercise nor diet influenced fat-free mass or RMR (kcal.m-2.h-1), both of which remained unchanged over time. A program similar to that followed by the ALX group is recommended for long-term weight control and overall health.

Adult↗

PubMed1999

The effects of age and dietary restriction without nutritional supplementation on whole bone structural properties in C57BL/6J mice.

While caloric restriction is a proven means to extend longevity, its effects on bone are not well understood. This study examined the effects of dietary restriction without vitamin or mineral supplementation on bone in female 60- and 120-day-old C57BL/6J mice. Baseline controls were sacrificed at 60 or 120 days, while diet-restricted animals ate approximately 72.9-78.6% of the ad libitum fed animals for thirty days. 60-day-old ad libitum animals experienced normal growth with average increases of 6.4% in bone length, 23.5% in bone mass, 9.4% in %mineralization, 36.4% in maximum strength, 59.2% in stiffness, 22.3% in cortical thickness, 12.9% in %cortical area, and 11.3% in microhardness. Growth in 120-day-old ad libitum animals followed a trend but with more modest increases. Diet-restricted mice matured very little from baseline levels in 60-day-old animals. There were no significant changes from baseline levels in the parameters indicated above, except for a 8.3% decrease in %cortical area attributable to increased resorption. 120-day-old diet-restricted animals also evidenced little deviation from baseline levels except for significant decreases in %mineralization (2.1%) and %cortical area (6.7%). The effects of diet restriction on bone properties decreased with age. Bone from 60-day-old diet-restricted mice showed diminished mechanical and compositional properties, resulting from little growth and excess resorption. Bone from 120-day-old diet-restricted mice showed little growth and some resorption. Increased resorption, localized on the endosteal surfaces, likely minimized the negative impact of structural degradation of the long bones. Resorption may have also provided minerals to compensate for nutritional deficiencies.

Aging↗

PubMed2006

The effect on health of alternate day calorie restriction: eating less and more than needed on alternate days prolongs life.

Restricting caloric intake to 60-70% of normal adult weight maintenance requirement prolongs lifespan 30-50% and confers near perfect health across a broad range of species. Every other day feeding produces similar effects in rodents, and profound beneficial physiologic changes have been demonstrated in the absence of weight loss in ob/ob mice. Since May 2003 we have experimented with alternate day calorie restriction, one day consuming 20-50% of estimated daily caloric requirement and the next day ad lib eating, and have observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette's, Meniere's) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes. We hypothesize that other many conditions would be delayed, prevented or improved, including Alzheimer's, Parkinson's, multiple sclerosis, brain injury due to thrombotic stroke atherosclerosis, NIDDM, congestive heart failure. Our hypothesis is supported by an article from 1957 in the Spanish medical literature which due to a translation error has been construed by several authors to be the only existing example of calorie restriction with good nutrition. We contend for reasons cited that there was no reduction in calories overall, but that the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH.

Caloric Restriction↗

PubMed1996

Calorie restriction lowers body temperature in rhesus monkeys, consistent with a postulated anti-aging mechanism in rodents.

Many studies of caloric restriction (CR) in rodents and lower animals indicate that this nutritional manipulation retards aging processes, as evidenced by increased longevity, reduced pathology, and maintenance of physiological function in a more youthful state. The anti-aging effects of CR are believed to relate, at least in part, to changes in energy metabolism. We are attempting to determine whether similar effects occur in response to CR in nonhuman primates. Core (rectal) body temperature decreased progressively with age from 2 to 30 years in rhesus monkeys fed ad lib (controls) and is reduced by approximately 0.5 degrees C in age-matched monkeys subjected to 6 years of a 30% reduction in caloric intake. A short-term (1 month) 30% restriction of 2.5-year-old monkeys lowered subcutaneous body temperature by 1.0 degrees C. Indirect calorimetry showed that 24-hr energy expenditure was reduced by approximately 24% during short-term CR. The temporal association between reduced body temperature and energy expenditure suggests that reductions in body temperature relate to the induction of an energy conservation mechanism during CR. These reductions in body temperature and energy expenditure are consistent with findings in rodent studies in which aging rate was retarded by CR, now strengthening the possibility that CR may exert beneficial effects in primates analogous to those observed in rodents.

Aging↗

PubMed2006

Health span extension by later-life caloric or dietary restriction: a view based on rodent studies.

In spite of the potential benefit of lifelong food restriction to retard aging and extend life span, it is unrealistic in human. The restriction late in life may be more practical. There are, however, only limited studies on the effect of late onset caloric or dietary restriction. We and other investigators have shown that the late life restriction rejuvenates some parameters that decline with age in rats and mice. Although such studies may provide a basis for human application of late-life caloric or dietary restriction, the prolongation of maximum life span would not be expected in view of the current status of the long-lived population in which maximum life span potential appears to have already been achieved. The late life caloric restriction, however, could extend the health span if the extent were appropriate.

Aging↗

PubMed1998

[Individualized cardiovascular prevention: when and how far should it go?].

Individualised cardiovascular prevention must primarily be applied to patients with coronary heart disease or another obvious atherosclerotic disease and to apparently healthy subjects, but presenting a high risk (which implies the detection of these subjects) and their close relatives. The European recommendations for the prevention of coronary heart disease in clinical practice have been recently up-dated. Calculation of the multifactorial absolute risk (probability of developing an event over a given period, taking into account all modifiable and non-modifiable risk factors) represents a decisional aid to intervene on lifestyle and drug prescription. However, the available tables and software require certain adjustments. Diet is a major determinant of the cardiovascular risk and has one of the most important, but most complex impacts on prevention. Restriction of saturated fats, a Mediterranean type of diet and caloric restriction in the case of obesity are the main objectives. Smoking cessation is essential. For all these measures, a specialist referral is too frequently neglected. Aerobic physical activity is recommended. Hypertension must be controlled regardless of age. The objective is to obtain blood pressure figures less than 140/90 mmHg, and even lower in the case of diabetes or renal disease. Evidence of the benefit of controlling hypercholesterolaemia has been reinforced and the objectives to be achieved have been redefined: in secondary prevention and in high-risk subjects, the target total cholesterol must be less than 1.90 g/l and LDL cholesterol must be less than 1.15 g/l. The control of all risk factors must be reinforced in diabetic patients and fasting blood glucose must be maintained between 0.91 and 1.20 g/l in insulin-dependent diabetic patients with coronary heart disease.

Cardiovascular Diseases↗

PubMed1992

Effects of voluntary exercise and/or food restriction on pancreatic tumorigenesis in male rats.

Studies were undertaken to evaluate the effects of caloric restriction on voluntary exercise in a rat model of pancreatic cancer. Suckling male Lewis rats were initiated with 3 doses (30 mg/kg body weight) of the pancreatic carcinogen azaserine. At 28 days of age they were weaned to one of four experimental protocols; namely, sedentary/ad libitum fed, voluntary exercise/ad libitum fed, sedentary/food restricted, and voluntary exercise/food restricted. Voluntary exercise was provided by free access to running wheels fitted with odometers. Food restriction was intended to be mild, at less than 10% reduction of ad libitum intake. Putative pre-neoplastic pancreatic foci were identified microscopically at 4 months post-azaserine treatment. As previously shown, food restriction led to increased wheel activity, but the increased activity could not be maintained beyond the first half of the post-initiation treatment phase. Additionally, the extensive wheel running occurred only when available food was restricted by greater than 10%. Exercise per se had a lesser effect compared to food restriction on pancreatic tumorigenesis.

Analysis of Variance↗