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PubMed2006

Effect of lipid restriction on mitochondrial free radical production and oxidative DNA damage.

Many studies have shown that caloric restriction (40%) decreases mitochondrial reactive oxygen species (ROS) generation in rodents. Moreover, we have recently found that 7 weeks of 40% protein restriction without strong caloric restriction also decreases ROS production in rat liver. This is interesting since it has been reported that protein restriction can also extend longevity in rodents. In the present study we have investigated the possible role of dietary lipids in the effects of caloric restriction on mitochondrial oxidative stress. Using semipurified diets, the ingestion of lipids in male Wistar rats was decreased by 40% below controls, while the other dietary components were ingested at exactly the same level as in animals fed ad libitum. After 7 weeks of treatment the liver mitochondria of lipid-restricted animals showed significant increases in oxygen consumption with complex I-linked substrates (pyruvate/malate and glutamate/malate). Neither mitochondrial H(2)O(2) production nor oxidative damage to mitochondrial or nuclear DNA was modified in lipid-restricted animals. Oxidative damage to mitochondrial DNA was one order of magnitude higher than that of nuclear DNA in both dietary groups. These results deny a role for lipids and reinforce the possible role of dietary proteins as being responsible for the decrease in mitochondrial ROS production and DNA damage in caloric restriction.

Animals↗

PubMedDate not supplied

Bone mineral density response to caloric restriction-induced weight loss or exercise-induced weight loss: a randomized controlled trial.

BACKGROUND: Bone loss often accompanies weight loss induced by caloric restriction (CR), but whether bone loss accompanies similar weight loss induced by exercise (EX) is unknown. We tested the hypothesis that EX-induced weight loss is associated with less bone loss compared with CR-induced weight loss. METHODS: Forty-eight adults (30 women; 18 men; mean +/- SD age, 57 +/- 3 years; and mean +/- SD body mass index, 27 +/- 2 kg/m2) were randomized to 1 of 3 groups for 1 year: CR group (n = 19), regular EX group (n = 19), or a healthy lifestyle (HL) control group (n = 10). Primary outcome measure was change in hip and spine bone mineral density (BMD). Secondary outcomes were bone markers and hormones. RESULTS: Body weight decreased similarly in the CR and EX groups (10.7% +/- 6.3% [-8.2 +/- 4.8 kg] vs 8.4% +/- 6.3% [-6.7 +/- 5.6 kg]; P = .21), whereas weight did not change in the HL group (-1.2% +/- 2.5% [-0.9 +/- 2.0 kg]). Compared with the HL group, the CR group had decreases in BMD at the total hip (-2.2% +/- 3.1% vs 1.2% +/- 2.1%; P = .02) and intertrochanter (-2.1% +/- 3.4% vs 1.7 +/- 2.8%; P = .03). The CR group had a decrease in spine BMD (-2.2% +/- 3.3%; P = .009). Despite weight loss, the EX group did not demonstrate a decrease in BMD at any site. Body weight changes correlated with BMD changes in the CR (R = 0.61; P = .007) but not in the EX group. Bone turnover increased in both CR and EX groups. CONCLUSIONS: CR-induced weight loss, but not EX-induced weight loss, is associated with reductions in BMD at clinically important sites of fracture. These data suggest that EX should be an important component of a weight loss program to offset adverse effects of CR on bone.

Alkaline Phosphatase↗

PubMed1992

Modulation of chemical toxicity by modification of caloric intake.

Caloric restriction increases maximum achievable lifespan and offsets the time to development of degenerative disease. Part of these desirable effects may result from positive modulation of toxic events. We have shown that when rodents are placed on a diet that is reduced in total calories by 40%, several beneficial changes on biochemical systems which impact on toxicologic processes are positively enhanced. Lipid metabolism is reduced and, therefore, the potential for lipoperoxidation is reduced. Additionally, activity of enzymes that produce free radicals as byproducts (cytochrome P4502C11) are also reduced. Concurrently, we have shown that the "effective" activity of catalase and the activity of superoxide dismutase (which are required for the detoxification of toxic oxygen radicals) are significantly increased by caloric restriction. The activities of enzymes of drug and xenobiotic metabolism are also altered by caloric restriction. The effect upon activity may be to either decrease or increase activity, dependent upon whether the enzyme activates compounds to intermediates which may be more toxic or whether the enzyme acts to reduce toxicity. We have also shown that caloric restriction may affect the initiation stage of carcinogenesis. Aflatoxin B1 binding to hepatic nuclear DNA was reduced by caloric restriction (caloric restriction reduced both major adducts that are formed upon exposure to aflatoxin B1). caloric restriction also reduced cytochrome P4502C11 which converts aflatoxin B1 to its toxic epoxide, and may partly explain the reduction in binding. These results suggest that caloric restriction may, in part, extend the time to development of degenerative disease by altering basic biochemical mechanisms of toxicity.

Animals↗

PubMed1997

Phase-advanced daily rhythms of melatonin, body temperature, and locomotor activity in food-restricted rats fed during daytime.

This study was performed to investigate possible effects of a timed caloric restriction on the light-dark (LD) synchronization of four biological rhythms pair-studied in the same animals. In Experiment 1, food-restricted rats kept under a photoperiod of 12 h light:12 h dark received 50% of previous ad libitum food 2 h after the onset of light. Their daily rhythm of pineal melatonin and rhythms of plasma melatonin and corticosterone were examined and compared to those of ad libitum control rats after 1 or 2 months of food restriction. A significant phase advance (about 2 h) was found for the pineal melatonin rhythm and for the daily onset of plasma melatonin. Timing of nocturnal peak of circulating corticosterone was unchanged, and a diurnal peak anticipated food presentation by about 2 h. In Experiment 2, effects of a timed caloric restriction under 12L:12D were studied on the expression of daily rhythms of body temperature and locomotor activity. To discriminate between the effects of timed meal feeding and those of the added caloric restriction, these rhythms were analyzed in food-restricted rats, as in Experiment 1, and were compared to those in sham-restricted rats, concomitantly fed twice more than food-restricted rats (i.e., a timed meal feeding without caloric restriction). Acrophase of the nocturnal peak of body temperature rhythm reached the greatest phase advance (7 h) in food-restricted rats, in which it was close to LD transition. The nocturnal component of locomotor activity rhythm also was markedly phase advanced (6 h) by caloric restriction, as indicated by wheel-running and general activity occurring form early afternoon to midnight. A smaller 4-h phase advance of the nocturnal peak of body temperature also was observed in sham-restricted rats, although the onset of locomotor activity rhythm apparently was unaffected by meal feeding and the end of activity rhythm was phase advanced by 2 h. These results indicate that timed caloric restriction is a potent phase-shifting agent that interacts with the LD cycle zeitgeber. This nonphotic stimulus phase advances melatonin, corticosterone, body temperature, and activity rhythms to different extents and thus suggests a change in the internal synchronization of the circadian system.

Animals↗

PubMed2006

Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage.

Many previous investigations have consistently reported that caloric restriction (40%), which increases maximum longevity, decreases mitochondrial reactive species (ROS) generation and oxidative damage to mitochondrial DNA (mtDNA) in laboratory rodents. These decreases take place in rat liver after only seven weeks of caloric restriction. Moreover, it has been found that seven weeks of 40% protein restriction, independently of caloric restriction, also decrease these two parameters, whereas they are not changed after seven weeks of 40% lipid restriction. This is interesting since it is known that protein restriction can extend longevity in rodents, whereas lipid restriction does not have such effect. However, before concluding that the ameliorating effects of caloric restriction on mitochondrial oxidative stress are due to restriction in protein intake, studies on the third energetic component of the diet, carbohydrates, are needed. In the present study, using semipurified diets, the carbohydrate ingestion of male Wistar rats was decreased by 40% below controls without changing the level of intake of the other dietary components. After seven weeks of treatment the liver mitochondria of the carbohydrate restricted animals did not show changes in the rate of mitochondrial ROS production, mitochondrial oxygen consumption or percent free radical leak with any substrate (complex I- or complex II-linked) studied. In agreement with this, the levels of oxidative damage in hepatic mtDNA and nuclear DNA were not modified in carbohydrate restricted animals. Oxidative damage in mtDNA was one order of magnitude higher than that in nuclear DNA in both dietary groups. These results, together with previous ones, discard lipids and carbohydrates, and indicate that the lowered ingestion of dietary proteins is responsible for the decrease in mitochondrial ROS production and oxidative damage in mtDNA that occurs during caloric restriction.

8-Hydroxy-2'-Deoxyguanosine↗

PubMedDate not supplied

Is the mitochondrial free radical theory of aging intact?

The present state of the mitochondrial free radical theory of aging is reviewed. Available studies do not support the hypothesis that antioxidants control the rate of aging because: (a) they correlate inversely with maximum longevity in vertebrates, and (b) increasing their concentration by different methods does not increase maximum lifespan. On the other hand, comparative studies consistently show that long-lived mammals and birds have low rates of mitochondrial reactive oxygen species (ROS) production and low levels of oxidative damage in their mitochondrial DNA. Furthermore, caloric restriction, which extends longevity, also decreases mitochondrial ROS production at complex I and lowers mtDNA oxidative damage. Recent data show that these changes can also be obtained with protein restriction without strong caloric restriction. Another trait of long-lived mammals and birds is the possession of low degrees of unsaturation in their cellular membranes. This is mainly due to minimizing the presence of highly unsaturated fatty acids such as 22:6n-3 and emphasizing the presence of less unsaturated fatty acids such as 18:2n-6 in long-lived animals, without changing the total amount of polyunsaturated fatty acids. This leads to lower levels of lipid peroxidation and lipoxidation-derived protein modification in long-lived species. Taken together, available information is consistent with the predictions of the mitochondrial free radical theory of aging, although definitive proof and many mechanistic details are still lacking.

Aging↗

PubMed2002

Effect of time of restriction on the decrease in mitochondrial H2O2 production and oxidative DNA damage in the heart of food-restricted rats.

In the present study, the question if medium-term (4 months) caloric restriction (40%) decreases mitochondrial H2O2 production and oxidative DNA damage was investigated. Caloric restriction (CR) is the only experimental manipulation that increases maximum life span. Previous long-term CR studies have showed that CR decreases the mitochondrial rate of free radical production in diverse tissues and species. Those studies agree with the idea that the superior longevity of the restricted animals can be partly due to their lower mitochondrial rate of free radical generation. However, caloric restriction effects strongly depend on implementation time. Previous studies have shown that the decrease induced by CR on oxygen radical generation and oxidative damage to mitochondrial DNA occurs after 1 year but not after 6 weeks of restriction. In the present investigation, mitochondrial H2O2 production did not change in medium-term (4 months) caloric restricted animals, and, in agreement with that, no differences were found in either mitochondrial or nuclear oxidative DNA damage between restricted and ad libitum-fed animals. These results confirm the importance of the time of CR implementation, and show that time longer than 4 months is needed to decrease the mitochondrial rate of free radical generation and the oxidative damage to mtDNA in the rat heart.

Animals↗

PubMed1985

Comparison of nicotinic acid- and caloric restriction-induced hyperbilirubinaemia in the diagnosis of Gilbert's syndrome.

The diagnostic value of the nicotinic acid (NA)-induced hyperbilirubinaemia was compared with that resulting from caloric restriction in 40 patients with Gilbert's syndrome (GS) and 20 controls. Both tests resulted in a significant higher level of serum bilirubin in GS than in controls (P less than 0.001). When the serum bilirubin level 240 min after NA administration (5.9 mumol/kg i.v.) was higher than 18 mumoles/l, this test had a specificity and sensitivity of 100%, both in males and females with the syndrome. The discriminatory value of the test was lower when either the area under the time concentration curve or the maximal increment of serum unconjugated bilirubin were used. Reduction in caloric intake (400 calories/day) showed a lower specificity and sensitivity than the NA test, particularly in females. An increment of bilirubin at 24 h greater than 15 mumoles/l was more diagnostic than an increase by 100% or more over the pre-diet value. The efficacy was not improved by prolonging the test for additional 24 h. From these data we conclude that NA-induced hyperbilirubinaemia and, in particular the concentration of the pigment 240 min after drug administration, is more efficient than fasting-induced hyperbilirubinaemia in the diagnosis of the Gilbert's syndrome both in males and in females.

Adult↗

PubMed1993

Expression of heat shock protein 70 is altered by age and diet at the level of transcription.

Because heat shock proteins have been shown to play a critical role in protecting cells from hyperthermia and other types of physiological stresses, it was of interest to determine what effect age and caloric restriction have on the ability of cells to regulate the expression of heat shock protein 70 (hsp70), the most prominent and most evolutionarily conserved of the heat shock proteins. Caloric restriction is the only experimental manipulation known to retard aging and increase survival of mammals. The ability of hepatocytes isolated from young/adult (4- to 7-month-old) and old (22- to 28-month-old) male Fischer F344 rats fed ad libitum or a caloric restriction diet (60% of the content of the ad libitum diet) to express hsp70 was determined after a mild heat shock (42.5 degrees C for 30 min). We found that the induction of hsp70 synthesis and mRNA levels by heat shock was 40 to 50% lower in hepatocytes isolated from old rats than in hepatocytes isolated from young rats. Using in situ hybridization, we found that essentially all hepatocytes from the young/adult and old rats expressed hsp70 in response to heat shock; therefore, the age-related decrease in the induction of hsp70 expression was not due to an age-related accumulation of cells that do not respond to heat shock. Measurements of hsp70 mRNA stability and hsp70 transcription demonstrated that the age-related decline in hsp70 expression arose from a decline in hsp70 transcription. Interestingly, the age-related decline in the induction of hsp70 expression was reversed by caloric restriction; e.g., the induction of hsp70 synthesis, mRNA levels, and nuclear transcription were significantly higher in hepatocytes isolated from old rats fed the caloric restricted diet than in hepatocytes isolated from old rats fed ad libitum. The levels of the heat shock transcription factor in nuclear extracts isolated from heat-shocked hepatocytes were measured in a gel shift assay. Binding of the heat shock transcription factor to the heat shock element decreased with age and was significantly higher in hepatocyte extracts isolated from old rats fed the caloric restriction diet than in those from old rats fed ad libitum. Thus, our study demonstrates that the ability of hepatocytes to respond to hyperthermia and express hsp70 decreases significantly with age and that this decrease occurs at the transcriptional level. In addition, caloric restriction, which retards aging, reversed the age-related decline in the induction of hsp70 transcription in hepatocytes.

Aging↗

PubMed2006

Moderate calorie restriction improves cardiac remodeling and diastolic dysfunction in the Dahl-SS rat.

Caloric restriction extends longevity and reduces the onset of chronic disease in many animal models. Recently, caloric restriction was shown in humans to be associated with lower blood pressure, decreased systemic inflammation, and improved cardiac diastolic parameters. However, the causation and mechanisms of caloric restriction were obscured by the varied diet composition of the participants. The Dahl salt-sensitive rat which develops gradual, hypertension-associated diastolic dysfunction was used in this study to assess the impact of caloric restriction upon decompensated pressure-overload hypertrophy. Male Dahl salt-sensitive rats were provided either a low-salt diet or a high-salt diet to initiate heart failure progression. A further subset of high-salt rats underwent 15% calorie restriction, with salt load held constant. Parameters measured included serial systolic blood pressure, body weight, and changes of left ventricular systolic and diastolic parameters and ventricular geometry by echocardiography. After 18 weeks, fasting glucose, blood lipids, heart weight, kidney weight, lung weight, plasma interleukin-6 and TNF-alpha, and cardiac lipid peroxidation were measured. Low-salt rats did not develop heart failure. While high-salt rats displayed features of decompensated pressure-overload hypertrophy, moderate calorie restriction remarkably reduced morbidity. Compared to the high-salt fed group, the high-salt, calorie-restricted group showed reduced blood pressure, delayed onset of cachexia, lower fasting hyperlipidemia, lower cardiac, renal and lung weight, less plasma IL-6 and TNF-alpha, less cardiac oxidative damage, and improved diastolic chamber function and cardiac index. Modest calorie restriction, independent of salt intake, reduced pathogenesis in this well described model of decompensated pressure-overload hypertrophy.

Animals↗

PubMed1998

Altered alveolar macrophage function in calorie-restricted rats.

Alveolar macrophage functions associated with clearance of bacteria from the lung were assessed in male Fischer 344 rats maintained on a 25% calorie-restricted diet. Calorie-restricted and ad libitum-fed (control) rats were exposed to concentrations of ozone known to compromise phagocytic function of alveolar macrophages. Ozone suppressed alveolar macrophage phagocytosis of latex beads in vitro in ad libitum-fed rats, but not in calorie-restricted rats. In fact, caloric restriction enhanced phagocytic function in both control and ozone-exposed animals. Ad libitum-fed rats exposed to ozone and challenged with Streptococcus zooepidemicus experienced a prolonged infection and influx of polymorphonuclear leukocytes (PMN), whereas calorie-restricted rats exposed to ozone cleared the bacteria in 24 h without an inflammatory response. Bacterial endotoxin-stimulated in vitro production of nitric oxide and tumor necrosis factor (TNF)-alpha as well as expression of TNF-alpha and interleukin-6 messenger RNAs were all lower in alveolar macrophages isolated from calorie-restricted rats. Together, the data suggest that caloric restriction enhances resistance to gram-positive bacteria, while lowering the production of proinflammatory mediators elicited by endotoxin, a component of gram-negative bacteria. Although increased bacterial resistance is considered beneficial, reduction in the lung's ability to induce inflammatory mediators can have both positive and pathophysiologic consequences.

Animals↗

PubMed2003

Dbh(-/-) mice are hypotensive, have altered circadian rhythms, and have abnormal responses to dieting and stress.

We used mice deficient in dopamine beta-hydroxylase [Dbh(-/-)] and their littermate controls [Dbh(+/-)] to examine the role of epinephrine (Epi) and norepinephrine (NE) in the maintenance of cardiovascular parameters during 7 days of caloric restriction and acute exposure to environmental stress. Cardiovascular parameters of the mice were monitored using blood pressure radiotelemeters at an ambient temperature of 29 degrees C. Under normal conditions, Dbh(-/-) mice had a low heart rate, were severely hypotensive, and displayed an attenuated circadian blood pressure rhythm. Upon 50% caloric restriction, Dbh(+/-) mice exhibited decreases in heart rate and mean blood pressure. However, the blood pressures of Dbh(-/-) mice did not fall significantly in response to caloric restriction, and the bradycardia associated with caloric restriction was attenuated in these mice. In response to an open-field test, the blood pressure and heart rate of Dbh(+/-) mice increased substantially and rapidly, whereas Dbh(-/-) mice had blunted changes in blood pressures and no change in heart rate. These data suggest a primary role of Epi and NE in mediating the hypotension induced by dieting. Furthermore, Epi and NE play a smaller, but still significant, role in the bradycardia induced by caloric restriction. In contrast, Epi and NE are required for the tachycardia in an open field but are not required for the increase in blood pressure.

Animals↗

PubMed1997

Cognitive effects of a long-term weight reducing diet.

OBJECTIVE: To investigate if long-term caloric restriction under controlled conditions adversely affects cognitive function in obese women. SUBJECTS: Healthy, premenopausal women between 23-42 y. Dieting group: n = 14. CONTROL GROUP: n = 11. DESIGN: Longitudinal weight loss study (repeated measures within-subject design) with 3 weeks of baseline, 15 weeks of 50% caloric restriction, and 3 weeks of weight stabilization. MEASUREMENTS: Computerized cognitive function tests (sustained attention, short-term memory, simple reaction time, motor performance and attentional focus), height, body weight, body composition (TOBEC) and behavioral questionnaires (Dutch Eating Behaviour Questionnaire, Eating Attitudes Test, and State-Trait Anxiety Inventory). RESULTS: Dieting women lost 12.3 +/- 5.5 kg (mean +/- s.d.) of body weight. Controlled long-term caloric restriction significantly slowed simple reaction time but did not diminish sustained attention, motor performance or immediate memory. Word recall performance significantly improved by 24% at the end of caloric restriction. CONCLUSIONS: The slowing of simple reaction time is a short-term and long-term consequence of caloric restriction. In contrast to previous short-term dieting studies, sustained attention and immediate memory were not impaired with long-term caloric restriction.

Adult↗

PubMed1984

Adipose tissue lipoprotein-lipase activity in obesity.

The activity of lipoprotein-lipase in heparin-eluates of adipose tissue (AT-LPLA) of three body regions was measured in 22 obese and 18 nonobese females under basal conditions. AT-LPLA in the obese women both before and after 10 d of caloric restriction was also measured. Basal LPLA correlated well with plasma insulin values and reduced significantly after caloric restriction. Relative body weight, body fat, fasting and glucose-stimulated insulin levels, triglycerides, total cholesterol, but not high-density lipoprotein cholesterol, significantly decreased after caloric restriction. Variation of insulin levels after caloric restriction was the best explanatory variable correlating with AT-LPLA variations. These results are consistent with a primary role of insulin in regulating AT-LPLA.

Adipose Tissue↗

PubMed1988

Mechanisms in obesity-related hypertension: role of insulin and catecholamines.

Although the association of obesity and hypertension is well recognized, the mechanisms involved in the pathogenesis of increased blood pressure in the obese are poorly understood. Recent studies addressing the impact of 1) body fat distribution on blood pressure and 2) dietary intake on sympathetic nervous system (SNS) activity suggest a plausible hypothesis that relates the hypertension of the obese to hyperinsulinemia and SNS stimulation. Hypertension in the obese is associated with fat accumulation in the upper body segments; this type of obesity is also characterized by hyperinsulinemia and insulin resistance. Insulin, moreover, is an important signal in the relationship between dietary intake and SNS activity: increased insulin levels are associated with SNS stimulation. The hyperinsulinemia of obesity may, therefore, increase blood pressure by 1) direct effects of insulin to stimulate renal sodium reabsorption, and 2) sympathetic stimulation of the heart, blood vessels, and kidney. Conversely, SNS suppression and diminished insulin following caloric restriction may explain the hypotensive effects of caloric restriction in obese hypertensive subjects. The hypothesis presented here emphasizes the important role of diet in the treatment of obese hypertensive subjects. The efficacy of caloric restriction, weight loss, and exercise in reducing blood pressure in the obese is linked to diminished insulin and SNS activity and may be viewed as evidence in favor of this hypothesis.

Blood Pressure↗

PubMed2006

Effects of three simultaneous demands on glucose transport, resting metabolism and morphology of laboratory mice.

In nature, animals must successfully respond to many simultaneous demands from their environment in order to survive and reproduce. We examined physiological and morphological responses of mice given three demands: intestinal parasite infection with Heligmosomoides polygyrus followed by caloric restriction (70% of ad libitum food intake versus ad libitum for 10 days) and/or cold exposure (5 degrees C vs. 23 degrees C for 10 days). We found significant interactions between these demands as well as independent effects. Small intestine structure and function changed with demands in both independent and interactive ways. Body mass decreased during caloric restriction and this decrease was greater for cold-exposed than warm-exposed mice. In ad libitum fed mice, body mass did not change with either cold exposure or parasite infection but body composition (fat versus lean mass of whole body or organs) changed with both demands. Generally, organ masses decreased with caloric restriction (even after accounting for body mass effects) and increased with cold exposure and parasite infection whereas fat mass decreased with both caloric restriction and parasite infection. Mass adjusted resting metabolic rate (RMR) increased with cold exposure, decreased with caloric restriction but, unlike previous studies with laboratory mice, did not change with parasite infection. Our results demonstrate that the ability of mice to respond to a demand is influenced by other concurrent demands and that mice show phenotypic plasticity of morphological and physiological features ranging from the tissue level to the level of the whole organism when given three simultaneous demands.

Animals↗

PubMed1986

Diet and carcinogenesis: historical perspectives.

Some 40-50 years ago, experiments with animals began to provide conclusive evidence that diet can significantly influence carcinogenesis. Underfeeding or severe restriction of caloric intake to between one-half and two-thirds of normal had a general inhibitory effect on development of tumors of various types. On the other hand, high fat diets were found to enhance tumor yields relative to low fat diets. The effect of dietary fat was shown to be independent of caloric intake and was more selective for certain types of tumors. Both dietary fat and caloric restriction appear to exert their effects mainly at the promotional stage of carcinogenesis, although the exact mechanisms are not known. Interest in the role of diet in carcinogenesis has been revived in recent years by epidemiologic data that show correlations between certain dietary constituents, such as dietary fat, and cancer incidence at particular sites in the body and mortality. These epidemiologic observations have, in turn, led to an increase in research on effects of diet on carcinogenesis in animal models.

Animals↗

PubMed2006

Time-dependent modulation of rat serum paraoxonase 1 activity by fasting.

High-density lipoprotein-associated paraoxonase 1 (PON1) protects the endothelium from the pro-oxidant activity of oxidised low-density lipoprotein. Whereas fasting has been related to increased oxidative stress, intermittent fasting and caloric restriction are associated to increased resistance to oxidative injury. Taking into consideration that serum PON1 activity is modulated by a restriction of caloric intake and because there is no evidence regarding PON1 response to total food deprivation, we investigated whether PON1 activity is involved in the response aimed to counteract the greater oxidative stress associated to fasting and whether serum PON1 activity is altered by the length of food deprivation. Male Wistar rats were randomly divided into five groups: fed and 6-, 12-, 24- or 48-h fasted rats. Serum PON1 activity increases within the first hours of fasting, representing a prompt adaptation designed to attenuate blood lipid peroxidation that cannot be sustained when fasting is prolonged. This PON1 response to early fasting could be part of the mechanisms triggered by periodically repeated short periods of food deprivation - intermittent fasting - which result in increased resistance to stress by stimulating antioxidant defences.

Animals↗