Beneficial Effects Of Fasting Research Articles

Intermittent Fasting Primes the Tumor Microenvironment and Improves Nanomedicine Delivery in Hepatocellular Carcinoma.

Fasting has many health benefits, including reduced chemotherapy toxicity and improved efficacy. It is unclear how fasting affects the tumor microenvironment (TME) and tumor-targeted drug delivery. Here the effects of intermittent (IF) and short-term (STF) fasting are investigated on tumor growth, TME composition, and liposome delivery in allogeneic hepatocellular carcinoma (HCC) mouse models. To this end, mice areinoculated either subcutaneously or intrahepatically with Hep-55.1C cells and subjected to IF for 24 d or to STF for 1 d. IF but not STF significantly slows down tumor growth. IF increases tumor vascularization and decreases collagen density, resulting in improved liposome delivery. In vitro, fasting furthermore promotes the tumor cell uptake of liposomes. These results demonstrate that IF shapes the TME in HCC towards enhanced drug delivery. Finally, when combining IF with liposomal doxorubicin treatment, the antitumor efficacy of nanochemotherapy isfound to be increased, while systemic side effects arereduced. Altogether, thesefindings exemplify that the beneficial effects of fasting on anticancer therapy outcomes go beyond modulating metabolism at the molecular level.

The Potential Benefits of Fasting Do Not Include Regenerative Stem Cells

Tracing back to the first civilizations, there has always been a drive to live longer healthier lives, to cheat death. As potions and prayers gave way to science, deeper understanding of the body’s chemicals and processes encouraged people to manipulate them in a quest to avoid disease. With the awareness and comprehension of stem cells, new questions arose, many of which were directed at how we might control stem cells that exist throughout the body to our benefit, or how we might utilize them to prevent or manage illness. An increasing number of studies appear to point to the ability of stem cells to regenerate through fasting, which could have potentially far-reaching implications in future approaches towards medical applications. The beneficial effects of fasting – though numerous – do not, however, include stem cell regeneration; instead, it is the cumulative effects of many of our body’s other mechanisms that tend to work together in rejuvenating cells of all types. Further, it is misleading to think that fasting will benefit every person in every situation, as it comes with its own complications and as such, is only recommended in very specific circumstances.

Complementary omics strategies to dissect p53 signaling networks under nutrient stress

Signaling trough p53is a major cellular stress response mechanism and increases upon nutrient stresses such as starvation. Here, we show in a human hepatoma cell line that starvation leads to robust nuclear p53 stabilization. Using BioID, we determine the cytoplasmic p53 interaction network within the immediate-early starvation response and show that p53 is dissociated from several metabolic enzymes and the kinase PAK2 for which direct binding with the p53 DNA-binding domain was confirmed with NMR studies. Furthermore, proteomics after p53 immunoprecipitation (RIME) uncovered the nuclear interactome under prolonged starvation, where we confirmed the novel p53 interactors SORBS1 (insulin receptor signaling) and UGP2 (glycogen synthesis). Finally, transcriptomics after p53 re-expression revealed a distinct starvation-specific transcriptome response and suggested previously unknown nutrient-dependent p53 target genes. Together, our complementary approaches delineate several nodes of the p53 signaling cascade upon starvation, shedding new light on the mechanisms of p53 as nutrient stress sensor. Given the central role of p53 in cancer biology and the beneficial effects of fasting in cancer treatment, the identified interaction partners and networks could pinpoint novel pharmacologic targets to fine-tune p53 activity.

Dysfunction of aged liver of male albino rats and the effect of intermitted fasting; Biochemical, histological, and immunohistochemical study

Intermittent fasting exerts beneficial effects on most age-related degenerative changes throughout the body. This study aimed to investigate the possible protective effects and mechanism of intermittent fasting on aged liver in male albino rats. Forty male albino rats were used in this study and were divided into four equal groups; Group I served as control ; rats aged 1 month sacrfied when they reached age of 4 month. Group II; rats aged 1 month with intermittent fasting for 3 months. The rats sacrfied when they reached age of 4 mounth Group III; rats aged 15-month fed an ad-libitum diet. The rats sacrified when they reached age of 18 month. Group IV; 15 month rats with intermittent fasting for 3 months. The rats sacrified when they reached age of 18 month. Liver specimens were excised and processed for biochemical, histological, and immunohistochemical study. Blood samples were collected for biochemical study. The result showed a significant increase in liver injury, oxidative stress, and inflammatory markers with a marked decrease in the autophagy marker in group III if compared with both group I and II. Additionally, group III showed hepatic vacuolations, cellular filtration, and congestion in both central and portal veins. A highly significant increase in the mean color intensity of positive immunochemical reaction for anti caspase 3 and anti-TNFα as well as a highly significant increase in the surface area fraction of collagen fibers were noticed in group III if compared with group I and II. Interestingly, intermittent fasting (group IV) remarkably reduced the previous alternation that that occurred in group III. It could be concluded that various biochemical, histological, and immunohistochemical alterations were observed in liver rat in group III. Beneficial effects of fasting on these changes were recorded in group IV through its anti-inflammatory, anti-apoptotic effect as well as its effect in modulating autophagy in aged liver cells. This might open the gate for further research and provide a new line for therapeutic intervention in aged liver. These data lead to speculate that sporadic fasting might represent a simple, safe, and inexpensive means to fight the changes occurred in the aged liver.

Outcomes of a Medically Supervised Fasting Module on Healthy Females in a Controlled Residential Environment: A Brief Report.

Background:Fasting is being used as a therapeutic and cultural practice for millennia. There are numerous reports available on beneficial effects of fasting on various disease conditions. Despite the mounting evidence on fasting, little is known on its physiological effects in humans as most of the studies on physiological effects are done in animals.Methods:Twenty healthy female volunteers (mean age ± SD, 21.95 ± 2.52 years) participated in a 10-day fasting program, which has 1 preparatory day and 1 refeeding day (1,000 kcal) and 8 fasting days (500 kcal). All the participants consented to participate in the study. Blood parameters like complete blood count, renal function test, total iron binding capacity, lipid profile, liver profile, vitamins D and B12, thyroid function tests, glycated hemoglobin, and air blood gas test along with anthropometric measurements were taken on the first and last day.Results:All the parameters under the study have shown statistically significant changes (p < 0.05) except hemoglobin (p = 0.7) and non-high density lipoprotein (p = 0.32). Notable changes were the significant increase in vitamins D and B12 levels that signifies the homoeostatic potential of a fasting regimen.Conclusion:The result depicts the positive impact of fasting on various physiological parameters that warrants further studies on the safety of fasting in diverse diseases, especially the ones that have metabolic disarray as the root cause. Despite the limitation of the smaller sample size and lack of a control group, the results are encouraging to devise disease-specific fasting programs.

Complementary Omics Strategies to Dissect p53 Signaling Networks Under Nutrient Stress

Signaling trough p53 is a major cellular stress response mechanism and increases upon nutrient stresses such as starvation. Here, we show in a human hepatoma cell line that starvation leads to robust nuclear p53 stabilization. Using BioID, we determine the cytoplasmic p53 interaction network within the immediate-early starvation response and show that p53 is dissociated from several metabolic enzymes and the kinase PAK2 for which direct binding with the p53 DNA-binding domain was confirmed with NMR studies. Furthermore, proteomics after p53 immunoprecipitation (RIME) uncovered the nuclear interactome under prolonged starvation, where we confirmed the novel p53 interactors SORBS1 (insulin receptor signaling) and UGP2 (glycogen synthesis). Finally, transcriptomics after p53 re-expression revealed a distinct starvation-specific transcriptome response and suggested previously unknown nutrient-dependent p53 target genes. Together, our complementary approaches delineate several nodes of the p53 signaling cascade upon starvation, shedding new light on the mechanisms of p53 as nutrient stress sensor. Given the central role of p53 in cancer biology and the beneficial effects of fasting in cancer treatment, the identified interaction partners and networks could pinpoint novel pharmacologic targets to fine-tune p53 activity.

Towards a fasting-mimicking diet for critically ill patients: the pilot randomized crossover ICU-FM-1 study

BackgroundIn two recent randomized controlled trials, withholding parenteral nutrition early in critical illness improved outcome as compared to early up-to-calculated-target nutrition, which may be explained by beneficial effects of fasting. Outside critical care, fasting-mimicking diets were found to maintain fasting-induced benefits while avoiding prolonged starvation. It is unclear whether critically ill patients can develop a fasting response after a short-term nutrient interruption. In this randomized crossover pilot study, we investigated whether 12-h nutrient interruption initiates a metabolic fasting response in prolonged critically ill patients. As a secondary objective, we studied the feasibility of monitoring autophagy in blood samples.MethodsIn a single-center study in 70 prolonged critically ill patients, 12-h up-to-calculated-target feeding was alternated with 12-h fasting on day 8 ± 1 in ICU, in random order. Blood samples were obtained at the start of the study, at the crossover point, and at the end of the 24-h study period. Primary endpoints were a fasting-induced increase in serum bilirubin and decrease in insulin requirements to maintain normoglycemia. Secondary outcomes included serum insulin-like growth factor I (IGF-I), serum urea, plasma beta-hydroxybutyrate (BOH), and mRNA and protein markers of autophagy in whole blood and isolated white blood cells. To obtain a healthy reference, mRNA and protein markers of autophagy were assessed in whole blood and isolated white blood cells of 23 matched healthy subjects in fed and fasted conditions. Data were analyzed using repeated-measures ANOVA, Fisher’s exact test, or Mann–Whitney U test, as appropriate.ResultsA 12-h nutrient interruption significantly increased serum bilirubin and BOH and decreased insulin requirements and serum IGF-I (all p ≤ 0.001). Urea was not affected. BOH was already increased from 4 h fasting onwards. Autophagic markers in blood samples were largely unaffected by fasting in patients and healthy subjects.ConclusionsA 12-h nutrient interruption initiated a metabolic fasting response in prolonged critically ill patients, which opens perspectives for the development of a fasting-mimicking diet. Blood samples may not be a good readout of autophagy at the tissue level.Trial registrationISRCTN, ISRCTN98404761. Registered 3 May 2017.

FASTING TECHNIQUES – CHANGING THE WAY, YOU LOOK AT THERAPY

At present, various complications such as diabetes, cardiovascular diseases, cancer, and neurological disorders have become treatable, almost completely, but the drugs used for the treatment may cause some severe side effects such as hypoglycemia, kidney complications, diarrhea, anemia, rashes, dyskinesia, insomnia, hypotension, confusion, hallucinations, compulsive behavior, and neurological complications. Some treatments cause defects in whole organ systems including damage to the immune system, lungs, heart, nerve endings, and reproductive organs. Many treatment approaches are using non-pharmacological techniques for treating diseases, without synthetic drugs. One such technique is fasting, a process where starvation conditions are imitated voluntarily. Intermittent fasting is done in ratios of fasting and food intake, where a person deprives himself of food for 16 h and food intake is followed for the rest of 8 h. Alternate day fasting includes alternate days of food intake and fasting. Time-restricted feeding is done by allowing food consumption only during the metabolically active phase of the day. Fasting mimicking diet is done by reducing food intake to very small levels which mimics the conditions of fasting. Reported beneficial effects of fasting have been found in diseases such as cancer, blood pressure disorders, autoimmune diseases, fibrosis, inflammation, insulin sensitivity, and oxidative stress.

Beneficial Effects of Fasting on White Adipose Tissue Inflammation and Metabolic Syndrome in Obese Subjects: Review

Beneficial Effects of Fasting on White Adipose Tissue Inflammation and Metabolic Syndrome in Obese Subjects: Review

Acute Fasting Regulates Retrograde Synaptic Enhancement through a 4E-BP-Dependent Mechanism

While beneficial effects of fasting on organismal function and health are well appreciated, we know little about the molecular details of how fasting influences synaptic function and plasticity. Our genetic and electrophysiological experiments demonstratethat acute fasting blocks retrograde synaptic enhancement that is normally triggered as a result of reduction in postsynaptic receptor function at the Drosophila larval neuromuscular junction (NMJ). This negative regulation critically depends on transcriptional enhancement of eukaryotic initiation factor 4E binding protein (4E-BP) under the control of the transcription factor Forkhead box O (Foxo). Furthermore, our findings indicate that postsynaptic 4E-BP exerts a constitutive negative input, which is counteracted by a positive regulatory input from the Target of Rapamycin (TOR). This combinatorial retrograde signaling plays a key role in regulating synaptic strength. Our results provide a mechanistic insight into how cellular stress and nutritional scarcity could acutely influence synaptic homeostasis and functional stability in neural circuits.

Effect of Ramadan fasting in Saudi Arabia on serum bone profile and immunoglobulins.

Each year Muslims fast from dawn to sunset for 1 month (Ramadan). In Saudi Arabia, the sleep-wake cycle during Ramadan is severely disturbed and is associated with abolition of the circadian cortisol rhythm, exposing Saudis to continuously increased cortisol levels, which may influence the immune response. In addition to cortisol, sleep and fasting affect the secretion of parathyroid hormone (PTH) and hence bone metabolism. Our objective was to investigate the effect of Ramadan type fasting on secretory patterns of PTH, markers of bone metabolism, and serum immunoglobulins. Blood samples from healthy young volunteers were collected at 9 a.m. and 9 p.m. (± 1 hour) before (Shaban) and 2 weeks into Ramadan. Calcium, phosphorus, magnesium, albumin, alkaline phosphatase, 25-OH vitamin D, intact PTH (iPTH), and immunoglobulin (Ig) A, M and G were measured. During Ramadan, evening-adjusted calcium was higher (p = 0.036) and phosphate lower (p < 0.001) than the corresponding morning value. Moreover, the Ramadan mean morning phosphate was higher and the evening level lower was than Shabaan values (p = 0.010 and p <0.001, respectively), while mean iPTH level was decreased compared with the morning value (p = 0.001), and the evening mean during Shabaan (p = 0.029). Mean IgG concentration was significantly lower during Ramadan (p = 0.003 and p = 0.021 for morning and evening, respectively). Changes in dietary practices during Ramadan modulated PTH secretion to a pattern which might be beneficial to bone health. Combined effects of fasting and disturbed sleep led to a noted decrease in IgG level. Therefore, a possible beneficial effect of fasting on bone turnover is combined with decreased immune response.

Role of mitochondrial permeability transition pore and mitochondrial ATP-sensitive potassium channels in the protective effects of ischemic preconditioning in isolated hearts from fed and fasted rats.

The aim of the present study was to assess whether the protective effects of ischemic preconditioning (PC) are associated with activation of the mitochondrial ATP-sensitive potassium channels (mitoKATP) and if there is any relationship between the activity of these channels and the mitochondrial permeability transition pore (MPTP) opening in ischemic-reperfused rat hearts under different nutritional conditions. Langendorff-perfused hearts of fed and 24-h fasted rats were exposed to 25 min of no-flow global ischemia plus 30 min of reperfusion. Fasting accelerated functional recovery and attenuated MPTP opening. The mitoKATP blocker, 5-hydroxydecanoic (HD), did not influence functional recovery and MPTP opening induced by ischemia-reperfusion in the fed hearts but partially reversed the beneficial effects of fasting. PC and the mitoKATP opener, diazoxide (DZ), improved functional recovery, preserved cell viability, and inhibited MPTP opening in both fed and fasted hearts. The protection elicited by PC and DZ on contractile recovery and MPTP opening was reversed by HD, which did not affect cell viability. Altogether, these results argue for a role of mitoKATP and its impact on preservation mitochondrial inner membrane permeability as a relevant factor in the improvement of contractile function in the ischemic-reperfused rat heart. They also suggest that the functional protection elicited by PC may be related to this mechanism.

OR13,76 Effects of metformin on hyperglycaemia-induced chemoresistance of DU145 and LNCaP prostate cancer cells

as amifostine, glutathione, mesna, and dexrazoxane have been investigated and shown to provide drug-dependent protection to specific tissues, but the use of these compounds has not been shown to increase disease-free or overall survival. We previously showed that fasting selectively protects mice, and possibly patients, but not tumors against high-dose chemotherapy (Differential Stress Resistance, DSR). Here we show that the beneficial effect of fasting extends beyond protecting normal cells to sensitizing malignant cells to chemotherapy. Further, we show that the differential protection of normal cells and sensitization of malignant cells by fasting is mediated by reduced IGF-I levels/signaling. A 72-hour fast provided remarkable protection against doxorubicin. We observed that fasting reduced circulating IGF-I by 70% and increased the level of the IGF-I inhibitor IGFBP-1 by 11-fold in mice. LID mice, with a 70–80% reduction in circulating IGF-I levels, were protected against 3 out of 4 chemotherapy drugs tested. Restoration of IGF-I during fasting was sufficient to reverse its protective effect. 60% of melanoma-bearing LID mice treated with doxorubicin reached long-term survival whereas all control mice died of either metastases or chemotoxicity. In both our fasted (72 hours) and LID mice, we observed a 40% decrease in IGFBP-3 levels. Therefore, to test if reduced IGFBP-3 levels mediated DSR, we challenge transgenic IGFBP-3 knockout mice (IGFBP3KO) with cyclophosphamide. We found no significant difference in survival between WT and IGFBP3KO mice, suggesting a larger role of IGF-I in mediating DSR independently of IGFBP-3. Reduction of IGF-I/IGF-I signaling protected primary glia, but not glioma cells against cyclophosphamide and protected mouse embryonic fibroblasts (MEFs) against doxorubicin-induced DNA damage. On the contrary, in malignant cells, the addition of IGF-I during fasting was sufficient to reverse the sensitization to chemotherapy in vitro. Similarly, S. cerevisiae lacking homologues of IGF-I signaling proteins displayed protection against chemotherapydependent DNA damage, which was reversed by expression of an oncogene homolog. Our studies suggest that fasting has the potential to protect patients and sensitize cancer cells, in part, by reducing IGF-I levels/signaling, thereby increasing the therapeutic index of toxic drugs commonly used in the treatment of a wide range of malignancies.

OR13,77 Insulin-like growth factors (IGFs) and IGF binding proteins in PSA-detected prostate cancer: a population-based case control study

as amifostine, glutathione, mesna, and dexrazoxane have been investigated and shown to provide drug-dependent protection to specific tissues, but the use of these compounds has not been shown to increase disease-free or overall survival. We previously showed that fasting selectively protects mice, and possibly patients, but not tumors against high-dose chemotherapy (Differential Stress Resistance, DSR). Here we show that the beneficial effect of fasting extends beyond protecting normal cells to sensitizing malignant cells to chemotherapy. Further, we show that the differential protection of normal cells and sensitization of malignant cells by fasting is mediated by reduced IGF-I levels/signaling. A 72-hour fast provided remarkable protection against doxorubicin. We observed that fasting reduced circulating IGF-I by 70% and increased the level of the IGF-I inhibitor IGFBP-1 by 11-fold in mice. LID mice, with a 70–80% reduction in circulating IGF-I levels, were protected against 3 out of 4 chemotherapy drugs tested. Restoration of IGF-I during fasting was sufficient to reverse its protective effect. 60% of melanoma-bearing LID mice treated with doxorubicin reached long-term survival whereas all control mice died of either metastases or chemotoxicity. In both our fasted (72 hours) and LID mice, we observed a 40% decrease in IGFBP-3 levels. Therefore, to test if reduced IGFBP-3 levels mediated DSR, we challenge transgenic IGFBP-3 knockout mice (IGFBP3KO) with cyclophosphamide. We found no significant difference in survival between WT and IGFBP3KO mice, suggesting a larger role of IGF-I in mediating DSR independently of IGFBP-3. Reduction of IGF-I/IGF-I signaling protected primary glia, but not glioma cells against cyclophosphamide and protected mouse embryonic fibroblasts (MEFs) against doxorubicin-induced DNA damage. On the contrary, in malignant cells, the addition of IGF-I during fasting was sufficient to reverse the sensitization to chemotherapy in vitro. Similarly, S. cerevisiae lacking homologues of IGF-I signaling proteins displayed protection against chemotherapydependent DNA damage, which was reversed by expression of an oncogene homolog. Our studies suggest that fasting has the potential to protect patients and sensitize cancer cells, in part, by reducing IGF-I levels/signaling, thereby increasing the therapeutic index of toxic drugs commonly used in the treatment of a wide range of malignancies.

The Effect of Ramadan Fasting on Hemoglobin, Hematocrit and Blood Biochemical Parameters

Background: Physicians in Islamic countries believe that fasting in Ramadan is equal to ingestion of thirty pills regularly ingested every year for clearing the blood and fortifying the tissues. The effects of Islamic fasting on physiologic functions in normal conditions have been considered in different studies and different topics. This study was to determine the quantitative changes of hemoglobin, hematocrit and certain serum biochemical parameters during Ramadan fasting in apparently healthy Muslim college students. Methods: Sixty-two students were followed in five stages: one week before, 3 rd , 15 th and 28 th day of Ramadan and ten days after Ramadan, by proper blood sampling in suitable time of day. Results: The findings showed a significant decrease in hemoglobin, glucose and uric acid on days 3 and 15 of Ramadan ( P P Conclusion: Changes in biochemical and hematological parameters of blood during Ramadan fasting are very important and the Islamic countries physicians should be informed about these beneficial effects of fasting. It seems that more researches are required for evaluating these effects in various physiologic and pathologic conditions and there are yet many unanswered questions in this relation. We believe that one of the physician responsibilities about patients is guiding and helping them for doing the religious duties in disease conditions because this has a great effect on recovery of patient. This consideration makes strong the physician-patient relationship.

Influence of Fasting on the Effects of Ischemic Preconditioning in the Ischemic-Reperfused Rat Heart

The effects of fasting and ischemic preconditioning (IP) on heart function of Langendorff-perfused rat hearts exposed to 25min global ischemia plus 30min reperfusion (RP), were correlated with lactate release and tissue-levels of long-chain acyl carnitine (LCCa) and CoA (LCCoA). IP was achieved by a 3min ischemia plus a 5min reperfusion cycle. Creatine kinase leakage was measured to assess the extent of cardiac injury. Fasting reduced the ischemic-induced contracture, improved RP recovery of mechanical function, reduced lactate release and increased the end-ischemia LCCoA and LCCa levels. Both in the fed and the fasted rat hearts IP delayed the pacemaker depression, reduced the amplitude of ischemic contracture and improved the RP recovery of contraction. However, IP reduced creatine kinase and lactate release only in the fed rat hearts. IP had no effects on tissue LCCa and LCCoA in both groups. These data suggest that: 1) beneficial effects of fasting may be ascribed, at least in part, to a reduced lactate production which may attenuate ischemic myocyte acidification and to the accumulation of fatty acyl esters which would favour citric acid cycle replenishment during RP. 2) beneficial effects of IP could be in part explained by the reduction of lactate production in the fed group although data obtained with the fasted rat heart indicate that another mechanisms must also be involved in the effects of IP. 3) accumulation of LCCoA and LCCa is not involved in the noxious effects of ischemia as well as in the protection effected by IP.

Influence of nutritional state on ischemic damage in rat liver.

The influence of the nutritional state of rats on the volume of necrosis in the liver at 24 h after 60 min ischemia has been estimated using fresh liver slices incubated in tetranitro BT. The volume of necrosis is about 30% in an animal fed ad libitum and about 10% in rats fasted for 24 h. Standardization of the time of feeding using a food dispensing apparatus did not reduce the relatively high individual variation in the extent of liver cell necrosis after ischemia. The beneficial effect of fasting on the extent of liver cell necrosis induced by ischemia may be due to decreased acidosis and/or a change in metabolic status.

Allergy of the External Ear and Canal

Intermittent fasting exerts beneficial effects on most age-related degenerative changes throughout the body. This study aimed to investigate the possible protective effects and mechanism of intermittent fasting on aged liver in male albino rats. Forty male albino rats were used in this study and were divided into four equal groups; Group I served as control ; rats aged 1 month sacrfied when they reached age of 4 month. Group II; rats aged 1 month with intermittent fasting for 3 months. The rats sacrfied when they reached age of 4 mounth Group III; rats aged 15-month fed an ad-libitum diet. The rats sacrified when they reached age of 18 month. Group IV; 15 month rats with intermittent fasting for 3 months. The rats sacrified when they reached age of 18 month. Liver specimens were excised and processed for biochemical, histological, and immunohistochemical study. Blood samples were collected for biochemical study. The result showed a significant increase in liver injury, oxidative stress, and inflammatory markers with a marked decrease in the autophagy marker in group III if compared with both group I and II. Additionally, group III showed hepatic vacuolations, cellular filtration, and congestion in both central and portal veins. A highly significant increase in the mean color intensity of positive immunochemical reaction for anti caspase 3 and anti-TNFα as well as a highly significant increase in the surface area fraction of collagen fibers were noticed in group III if compared with group I and II. Interestingly, intermittent fasting (group IV) remarkably reduced the previous alternation that that occurred in group III. It could be concluded that various biochemical, histological, and immunohistochemical alterations were observed in liver rat in group III. Beneficial effects of fasting on these changes were recorded in group IV through its anti-inflammatory, anti-apoptotic effect as well as its effect in modulating autophagy in aged liver cells. This might open the gate for further research and provide a new line for therapeutic intervention in aged liver. These data lead to speculate that sporadic fasting might represent a simple, safe, and inexpensive means to fight the changes occurred in the aged liver.