Chronic starvation and its associated metabolic derangements are known to have dangerous cardiovascular implications in the long term, but less is known about the cardiovascular consequences of acute starvation, such as in the context of a hunger strike. This case describes a patient who presented with signs and symptoms of acute coronary syndrome which began two weeks into a hunger strike and was ultimately found to have stress cardiomyopathy with complete resolution on subsequent imaging.

Short-term starvation (STS) during chemotherapy can block the nutrient supply to tumors and make tumor cells much more sensitive to chemotherapeutic drugs than normal cells. However, because of the diversity of starvation methods and the heterogeneity of tumors, this method\'s specific effects and mechanisms for chemotherapy are still poorly understood. In this study, we used HeLa cells as a model for short-term starvation and etoposide (ETO) combined treatment, and we also mimicked the short-term starvation effect by knocking down the glycolytic enzyme GAPDH to explore the exact molecular mechanism. In addition, our study demonstrated that short-term starvation protects cancer cells against the chemotherapeutic agent ETO by reducing DNA damage and apoptosis due to the STS-induced cell cycle G1 phase block and S phase reduction, thereby diminishing the effect of ETO. Furthermore, these results suggest that starvation therapy in combination with cell cycle-specific chemotherapeutic agents must be carefully considered.

Since its discovery in the late 19th century, radiotherapy has been one of the most important medical treatments in oncology. Recently, fasting or short-term starvation (STS) in cancer patients undergoing chemotherapy has been studied to determine its potential for enhancing the therapeutic index and for preventing side- effects, but no data are available in the radiotherapy setting. We thus decided to investigate the effects in vitro of STS in combination with radiotherapy in metastatic cancer cells and non-cancer cells.
Cells were incubated in short-term starvation medium (STS medium, 0·5 g/L glucose + 1% FBS) or in control medium (CM medium, 1 g/L glucose + 10 % FBS) for 24 h and then treated with single high-dose radiation. A plexiglass custom-built phantom was used to irradiate cells. DNA damage was evaluated using alkaline comet assay and theCometAnalyser software. The cell surviving fraction was assessed by clonogenic assay.
STS followed by single high-dose radiation significantly increased DNA damage in metastatic cancer cell lines but not in normal cells. Furthermore, STS reduced the surviving fraction of irradiated tumor cells, indicating a good radio-sensitizing effect on metastatic cell lines. This effect was not observed in non-tumor cells.
Our results suggest that STS may alter cellular processes, enhancing the efficacy of radiotherapy in metastatic cancer cellsin vitro. Interestingly, STS has radioprotective effect on the survival of healthy cells.

Previous research has shown that short-term fasting in healthy individuals is associated with changes in risky decision-making. The current experiment was designed to examine the influence of short-term fasting in healthy individuals on four types of impulsivity: reflection impulsivity, risky decision-making, delay aversion, and action inhibition. Participants were tested twice, once when fasted for 20 h, and once when satiated. Participants demonstrated impaired action inhibition when fasted; committing significantly more errors of commission during a food-related Affective Shifting Task. Participants also displayed decreased reflection impulsivity when fasted, opening significantly more boxes during the Information Sampling Task (IST). There were no significant differences in performance between fasted and satiated sessions for risky decision-making or delay aversion. These findings may have implications for understanding eating disorders such as Bulimia Nervosa (BN). Although BN has been characterized as a disorder of poor impulse control, inconsistent findings when comparing individuals with BN and healthy individuals on behavioral measures of impulsivity question this characterization. Since individuals with BN undergo periods of short-term fasting, the inconsistent findings could be due to differences in the levels of satiation of participants. The current results indicate that fasting can selectively influence performance on the IST, a measure of impulsivity previously studied in BN. However, the results from the IST were contrary to the original hypothesis and should be replicated before specific conclusions can be made.

The branched-chain amino acids (BCAA) play an important role in muscle energy metabolism, and Krüppel-like factor 15 (KLF15) is an essential regulator of BCAA metabolism in muscle under nutritional deficiency. In this study, we analyzed the effect of normal feeding (starvation for 0 day), starvation for 3, 7, 10, 15 days, and refeeding for 7 days after 15 days of starvation on the expression of KLF15 and BCAA metabolism in muscle of Chinese soft-shelled turtles by a fasting-refeeding trial. The results showed that the level of KLF15 transcription was increased first and then decreased in muscle during short-term starvation, and the protein level was gradually increased. Both the mRNA and protein level of the KLF15 returned to normal feeding level after refeeding for 7 days. The changing trend of the activities of branched-chain aminotransferase (BCAT) and alanine aminotransferase (ALT) was consistent to that of KLF15 mRNA, but at the transcription level, the expression of BCAT mRNA was consistent with the change of enzyme activity as well as ALT continued to increase in muscle under starvation. In addition, BCAA content showed a trend that decreased first and then increased under starvation, while the alanine (Ala) was the contrary. The above results indicated that the regulatory role of KLF15 in BCAA catabolism of muscle in Chinese soft-shelled turtles under nutritional deficiency, which might be activated the catabolism of BCAA in muscle to provide energy and maintain the homeostasis by KLF15-BACC signaling axis.

The glucose transporters (GLUTs) are well known for their essential roles in moving the key metabolites, glucose, galactose, fructose and a number of other important substrates in and out of cells. In this study, we identified a total of 21 glut genes in spotted sea bass (Lateolabrax maculatus) through extensive data mining of existing genomic and transcriptomic databases. Glut genes of spotted sea bass were classified into three subfamilies (Class I, Class II and Class III) according to the phylogenetic analysis. Glut genes of spotted sea bass were distributed in 15 out of 24 chromosomes. Deduced gene structure analysis including the secondary structure and the three-dimensional structures, as well as the syntenic analysis further supported their annotations and orthologies. Expression profile in healthy tissues indicated that 9 of 21 glut genes were expressed in liver of spotted sea bass. During short-term starvation, the mRNA expression levels of 3 glut genes (glut2, glut5, and glut10) were significantly up-regulated in liver (P < 0.05), indicating their potential roles in sugar transport and consumption. These findings in our study will facilitate the further evolutionary characterization of glut genes in fish species and provide a theoretical basis for their functional study.

To survive and reproduce, living organisms must evolve numerous mechanisms to re-adjust their physiology when encountering adverse conditions that subject them to severe stress. We found that short-term starvation (STS) stress in young adult male Caenorhabditis elegans can significantly improve their vitality (relative to nonstressed males) when they are aged. In addition, we found that stress-treated aged males maintained reproductive activity equivalent to young males, whereas nonstressed aged males quickly lost reproductive ability. STS stress can preserve sperm number and quality in aged male worms. Spermatogenesis involves germ cell mitosis and meiosis. We found that germ cell meiotic activity is more sensitive to aging than mitotic activity and is declining rapidly with age. We examined the role of numerous factors important for spermatogenesis on STS-preserved spermatogenesis during aging. Our results show that mutant strains deficient in anaphase-promoting complex/cyclosome (APC/C) function fail to exhibit the STS stress-enhanced spermatogenesis found in wild-type N2 worms, suggesting that the mechanism underlying starvation-induced spermatogenesis involves the APC/C complex, a conserved ubiquitin-protein ligase E3 complex. Furthermore, transgenic expression of FZY-1/CDC-20, a coactivator of APC/C, ameliorated the age-associated decline of meiosis, similar to the hormetic effect of STS.

Motilin (MLN), an interdigestive hormone secreted by endocrine cells of the intestinal mucosa, binds to a G protein-coupled receptor to exert its biological function of regulating gastrointestinal motility. In the present study, we identified the prepromotilin and mln receptor (mlnr) from the spotted sea bass, Lateolabrax maculatus. Mln consisted of an ORF of 336 nucleotides encoding 111 amino acids. The precursor protein contained a 17-amino-acid mature peptide. Mlnr had an ORF of 1089 bp encoding a protein of 362 amino acids. Seven transmembrane domains were predicted with TMHMM analysis. The phylogenetic analysis of mln and mlnr showed that they fell into the same clade with respective counterpart of selected fishes before clustering with other detected vertebrates. Both mln and mlnr genes were highly expressed in intestine of spotted sea bass using quantitative real-time PCR. In situ hybridization indicated that mln and mlnr mRNA were both localized in the lamina propria and the epithelial cell of intestinal villus. The expressions of both genes were regulated under short-term starvation in a time-dependent manner. In vitro experiments indicated that the expressions of ghrelin (ghrl), gastrin (gas) and cholecystokinin (cck) were enhanced by MLN after 3-h treatment, but the effect was absent after 6 or 12-h incubation. Taken together, the MLN and its receptor might play important roles in regulating intestinal motility in spotted sea bass.

Patients with malignant gliomas have a poor prognosis. Diets that lower blood glucose, such as ketogenic or caloric restricted diets (KCRDs), are hypothesized to reduce tumor growth and improve survival. In this systematic review, we summarize preclinical and clinical data on KCRDs in gliomas.
We searched PubMed and Embase for preclinical and clinical studies on KCRDs in gliomas, and extracted data on surrogate and clinically relevant endpoints, in accordance with PRISMA statement. Quality assessment of clinical studies was performed with use of Cochrane Collaboration\'s tool. We performed Fisher\'s exact test to examine associations between surrogate and clinically relevant endpoints.
We included 24 preclinical studies, seven clinical studies and one mixed study. Both preclinical and clinical studies were highly heterogeneous. Preclinically, KCRDs reduced tumor growth, but only a small majority of the in vivo studies found improved survival. These effects were stronger in groups with decreased blood glucose than in those with increased ketones, and also when other therapies were used concomitantly. Finally, KCRDs influence multiple molecular-biological pathways, including the PTEN/Akt/TSC2 and NF-kB pathway. In clinical studies, KCRDs seem to be safe and feasible in glioma patients. Clinical data were insufficient to draw conclusions regarding efficacy.
KCRDs have positive effects on malignant gliomas in published preclinical studies. Preliminary clinical data suggest that KCRDs are safe and feasible. However, because of the paucity of clinical data, the efficacy of KCRDs for improving survival and quality of life of glioma patients remains to be proven in prospective studies.

Objective: To investigate the role of short-term starvation (STS) in alleviating hepatic ischemia-reperfusion injury in mice and possible mechanism of action. Methods: Wild-type male C57BL/6 mice aged 8 weeks were randomly divided into 75% hepatic ischemia-reperfusion injury group (IR group), STS+75% hepatic ischemia-reperfusion injury group (STS group), and sirtinol+STS+75% hepatic ischemia-reperfusion injury group (SIR group), using a random number table, and sham-operation groups (IR-Sham group, STS-Sham group, and SIR-Sham group) were also established. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured, and the histomorphological changes of the liver were observed, as well as the expression of Sirt1, LC3B, and P62 proteins in liver tissue and the results of LC3B fluorescence staining. An analysis of variance was used for comparison of data between multiple groups, and the t-test was used for comparison of data between two groups. Results: Compared with the IR group, the STS group had significant reductions in the serum levels of ALT (3 152.7 ± 735.6 U/L vs 8 414.2 ± 1 052.2 U/L, P < 0.01) and AST (3 577.0 ± 714.0 U/L vs 10 845.8 ± 1 145.7 U/L, P < 0.01) and significant alleviation of liver pathological injury (Suzuki score: 1.50±0.55 vs 3.50±0.55, P < 0.01). Compared with the STS group, the SIR group had significant increases in the serum levels of ALT (7 002.7 ± 1 485.2 U/L vs 3 152.7 ± 735.6 U/L, P < 0.01) and AST (8 980.7 ± 1 739.1 U/L vs 3 577.0 ± 714.0 U/L, P < 0.01) and significant exacerbation of liver pathological injury (Suzuki score: 3.33 ± 0.52 vs 1.50 ± 0.55, P < 0.01). Compared with the IR group and the IR-Sham group, the STS group and the STS-Sham group had significant increases in the mRNA and protein expression of Sirt1 and the protein expression of LC3B and a significant reduction in the protein expression of P62, as well as a significant increase in the percentage of LC3B-positive cells in liver tissue (22.83% ± 5.19% / 22.17% ± 4.83% vs 10.16% ± 3.06% / 10.83% ± 1.94%, both P < 0.01). Compared with the STS group and the STS-Sham group, the SIR group and the SIR-Sham group had significant reductions in the expression of Sirt1 and LC3B proteins and a significant increase in the expression of P62 protein, as well as a significant reduction in the percentage of LC3B-positive cells in liver tissue (11.83% ± 9.24% / 14.67% ± 4.68% vs 22.83% ± 5.19% / 22.17% ± 4.83%, both P < 0.01). Conclusion: STS can effectively alleviate hepatic ischemia-reperfusion injury, and its protective effect may be associated with increasing the expression of Sirt1, inducing and promoting hepatocyte autophagy, and reducing hepatocyte death.
目的： 观察短期禁食对小鼠肝脏缺血再灌注损伤的作用，并探索其作用机制。 方法： 将8周龄野生型C57BL/6雄性小鼠按照数字随机法分为75%肝缺血再灌注（IR）损伤组（IR组）、短期禁食+ 75%肝IR损伤组（STS组）、sirtinol +短期禁食+ 75%肝IR损伤组（SIR组），并分别设立假手术组（IR-Sham组、STS-Sham组和SIR-Sham组）。检查各组小鼠血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）水平、肝组织形态学改变情况，及肝组织沉默信息调节因子2相关酶1（Sirt1）、微管相关蛋白1轻链3B （LC3B）、P62蛋白表达情况与LC3B荧光染色情况。多组数据比较采用方差分析法，两组间数据比较用t检验。 结果： 与IR组相比，STS组小鼠ALT [（3 152.7±735.6）U/L与（8 414.2±1 052.2）U/L，t = 10.00，P < 0.01]和AST[（3 577.0±714.0）U/L与（10 845.8±1 145.7）U/L，t = 13.19，P < 0.01]水平均显著降低；肝组织病理学损伤明显减轻（Suzuki评分为1.50±0.55与3.50±0.55，t = 6.33，P < 0.01）；而SIR组ALT [（7 002.7±1 485.2）U/L]和AST [（8 980.7±1 739.1）U/L]水平再次升高，与STS组相比，差异均有统计学意义[t = 5.69, P < 0.01（ALT）; t = 7.04, P < 0.01（AST）]，病理学损伤也较STS组明显加重（Suzuki评分为3.33±0.52与1.50±0.55，t = 5.97, P < 0.01）。STS组及STS-Sham组肝组织中Sirt1基因及蛋白表达水平分别较IR组及IR-Sham组明显提高，LC3B蛋白表达水平明显提高，P62蛋白表达水平明显下降，LC3B染色阳性细胞比率明显升高（22.83%±5.19%与10.16%±3.06%，t = 5.15，P < 0.01; 22.17%±4.83%与10.83%±1.94%，t = 5.33, P < 0.01）；而在SIR组及SIR-Sham组肝组织中，Sirt1表达水平较STS组及STS-Sham组显著下降，LC3B蛋白表达水平显著下降，P62蛋白表达水平显著提高，LC3B染色阳性细胞比率明显下降（11.83%±9.24%与22.83%±5.19%，t = 2.54，P = 0.029；14.67%±4.68%与22.17%±4.83%，t = 2.73，P = 0.021）。 结论： 短期禁食可有效减轻肝脏IR损伤。其对肝脏的保护作用可能与增加Sirt1表达及诱导、促进肝组织细胞自噬、减少肝细胞死亡有关。.