Environmental stresses play critical roles in the physiology of crustaceans. Food deprivation is an important environmental factor and a regular occurrence in both natural aquatic habitats and artificial ponds. However, the underlying physiological response mechanisms to starvation-caused stress in crustaceans are yet to be established. In the present study, the hepatopancreas tissue of Macrobrachium nipponense was transcriptome analyzed and examined for starvation effects on oxidative stress, DNA damage, autophagy, and apoptosis across four fasting stages (0 (control group), 7, 14, and 21 days). These results indicated that a ROS-mediated regulatory mechanism is critical to the entire fasting process. At the initial stage of starvation (fasting 0 d ~ 7 d), ROS concentration increased gradually, activating antioxidant enzymes to protect the cellular machinery from the detrimental effects of oxidative stress triggered by starvation-induced stress. ROS content production (hydrogen peroxide and superoxide anion) then rose continuously with prolonged starvation (fasting 7 d ~ 14 d), reaching peak levels and resulting in autophagy in hepatopancreas cells. During the final stages of starvation (fasting 14 d ~ 21 d), excessive ROS induced DNA damage and cell apoptosis. Furthermore, autophagolysosomes and apoptosis body were further identified with transmission electron microscopy. These findings lay a foundation for further scrutiny of the molecular mechanisms combating starvation-generated stress in M. nipponense and provide fishermen with the theoretical guidance for adopting fasting strategies in M. nipponense aquaculture.

Compensatory growth (CG) is a physiological response that accelerates growth following a period of nutrient limitation, with the potential to improve growth efficiency and meat quality in cattle. However, the underlying molecular mechanisms remain poorly understood. In this study, 60 Huaxi cattle were divided into one ad libitum feeding (ALF) group and two restricted feeding groups (75% restricted, RF75; 50% restricted, RF50) undergoing a short-term restriction period followed by evaluation of CG. Detailed comparisons of growth performance during the experimental period, as well as carcass and meat quality traits, were conducted, complemented by a comprehensive transcriptome analysis of the longissimus dorsi muscle using differential expression analysis, gene set enrichment analysis (GSEA), gene set variation analysis (GSVA), and weighted correlation network analysis (WGCNA). The results showed that irrespective of the restriction degree, the restricted animals exhibited CG, achieving final body weights comparable to the ALF group. Compensating animals showed differences in meat quality traits, such as pH, cooking loss, and fat content, compared to the ALF group. Transcriptomic analysis revealed 57 genes and 31 pathways differentially regulated during CG, covering immune response, acid-lipid metabolism, and protein synthesis. Notably, complement-coagulation-fibrinolytic system synergy was identified as potentially responsible for meat quality optimization in RF75. This study provides novel and valuable genetic insights into the regulatory mechanisms of CG in beef cattle.

LPXRFa, also known as gonadotropin-inhibitory hormone (GnIH), and kisspeptin (Kiss) are two major hypothalamic peptides that modulate the reproductive axis of vertebrates, including teleosts. However, little information is available regarding the actions of nutritional status on the regulation of these two neuroendocrine systems in fish. Herein, we assessed the effects of starvation and refeeding on the expression of lpxrfa, kiss2 and their receptors (lpxrfa-r and kiss2r respectively) at the brain-pituitary level of half-smooth tongue sole (Cynoglossus semilaevis). Food deprivation for 4 weeks induced a rise in brain lpxrfa as well as brain and pituitary lpxrfa-r mRNA levels, and refeeding restored brain lpxrfa and lpxrfa-r expression back to normal. However, pituitary lpxrfa-r mRNA levels still remained high after 1 week of refeeding. Neither lpxrfa nor kiss2 transcripts in the pituitary were altered by fasting, but their mRNA levels increased significantly after 1 week of refeeding, and declined back to the control levels after 2 weeks of refeeding. None of brain kiss2 and kiss2r along with pituitary kiss2r transcripts were modified by the nutritional status. In summary, our results revealed an interaction between energy status and the elements of LPXRFa and Kiss systems in the brain-pituitary axis of half-smooth tongue sole. Food deprivation and refeeding differentially regulated the two systems, which provided additional evidence for the involvement of the LPXRFa and Kiss systems in the regulation of reproduction by energy balance in non-mammalian species.

Releasing juvenile fish into resource-depleted waters is regarded as an effective way to restore fishery resources. However, during this stage, released fish are most vulnerable to long-term food deprivation due to environmental changes and low adaptability. Therefore, research regarding the energy regulation of fish under starvation stress is crucial to the optimization of release strategies. In this study, we performed a transcriptome analysis of the liver of Onychostoma sima subjected to starvation for 14 days. The results showed that, under long-term starvation, the liver regulated glucose homeostasis by activating the gluconeogenesis pathway. Meanwhile, the fatty acid metabolism pathway was activated to supply acetyl-coA to the TCA cycle, thus increasing mitochondrial ATP production and maintaining the balance of energy metabolism. Nevertheless, the activation of energy metabolism could not completely compensate for the role of exogenous nutrients, as evidenced by the downregulation of many genes involved in antioxidant defenses (e.g., cat, gpx3, mgst1, and mgst2) and immune response (e.g., c3, cd22, trnfrsf14, and a2ml). In summary, our data reveal the effects of long-term starvation on the energy metabolism and defensive regulation of starved juvenile fish, and these findings will provide important reference for the optimization of artificial release.

Salamanders are unique among tetrapods in their ability to regenerate their limbs throughout life. Like other poikilothermic amphibians, salamanders also show a remarkable capacity to survive long periods of starvation. Whether the physiological reserves necessary for tissue regeneration are preserved or sacrificed in starved salamanders is unknown. In the current study, we maintained Iberian ribbed newts ( Pleurodeles waltl) under extreme physiological stress to assess the extent of regeneration and identify the molecular and cellular changes that may occur under such conditions. After 19 months of complete food deprivation, the animals exhibited extensive morphological and physiological adaptations but remained behaviorally active and vigilant. Autophagy was elevated in different tissues and the transformed gut microbiota indicated remodeling of the intestinal tract related to autophagy. Upon limb amputation in animals starved for 21 months, regeneration proceeded with progenitor cell proliferation and migration, leading to limb blastema formation. However, limb outgrowth and patterning were substantially attenuated. Blockage of autophagy inhibited cell proliferation and blastema formation in starved animals, but not in fed animals. Hence, tissue autophagy and the regenerative response were tightly coupled only when animals were under stress. Our results demonstrate that under adverse conditions, salamanders can exploit alternative strategies to secure blastema formation for limb regeneration.
两栖类蝾螈具有独特的肢体再生能力。与其他两栖类动物类似，蝾螈也拥有极强的饥饿耐受能力。在饥饿的蝾螈体内，肢体再生是否能正常进行，禁食后蝾螈如何利用物质储存来促进再生还不得而知。我们对西班牙肋突螈 ( Pleurodeles waltl) 进行长期禁食处理，使其处于极端饥饿的状态，然后检测其断肢再生能力。经过长达近两年的禁食，动物形态与生理状态都发生了显著的变化，但仍能保持正常机体功能。禁食动物各种组织内的自噬水平都有所上升，肠道微生物的重塑也与细胞自噬相关。对禁食的动物进行截肢手术后，发生了大量细胞增殖并生成了再生芽基，但是再生的速率比正常喂食组有所减弱。在禁食动物中抑制自噬，能够减缓细胞增殖与再生芽基生成，而自噬抑制对正常饲喂动物的再生过程没有影响。因此，只有在动物处于禁食压力下，细胞自噬对断肢再生才是必须的。而在正常情况下，蝾螈的肢体再生不需要细胞自噬。我们的结果证明了当蝾螈处于不利条件下，其仍能通过动用其他替代途径为肢体再生提供所需的物质与能量。.

BACKGROUND: The association between childhood food deprivation (FD) and health in later life has been extensively studied; however, studies on the association between childhood food deprivation and frailty are scarce. This study assessed the associations between childhood FD and the risk of frailty at middle-age and old age.
METHODS: Three waves of the China Health and Retirement Longitudinal Study (CHARLS), including 11,615 individuals aged over 45 years, were used for this research. Frailty was operationalized according to the FRAIL scale as a sum of fatigue, resistance, ambulation, illness, and the loss of weight. Childhood FD experiences and levels were measured by self-reported FD and historical content. Logistic mixed-effects models and proportional odds ordered logistic regression models were used to analyse the association between childhood FD and frailty.
RESULTS: Childhood FD increased the odds of frailty at old age (1.30, 95% CI: 1.26-1.36). Compared with subjects with mild FD, those with extreme FD experiences had increased risks of frailty (1.34, 95% CI: 1.26-1.43). Subjects exposed to hunger at different ages all had an increased risk of frailty, and subjects who had FD during ages 6-12 (1.15, 95% CI: 1.09-1.22) were more likely to have an increased risk of frailty than those who had experienced FD in younger ages. The interaction of experience of FD at ages 0-6 and the experience of FD at ages 6-12 is not statistically significant after adjusting all covariates.
CONCLUSIONS: Our findings suggest that childhood FD exerts long-lasting effects on frailty among older adults in China. The prevention of childhood FD may delay or even avert the emergence of frailty in people of middle-age and old age.

The black carp (Mylopharyngodon piceus) is an important carnivorous freshwater-cultured species. To understand the molecular basis underlying the response of black carp to fasting, we used RNA-Seq to analyze the liver and brain transcriptome of fasting fish. Annotation to the NCBI database identified 66,609 unigenes, of which 22,841 were classified into the Gene Ontology database and 15,925 were identified in the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Comparative analysis of the expression profile between fasting and normal feeding fish revealed 13,737 differentially expressed genes (P < 0.05), of which 12,480 were found in liver tissue and 1257 were found in brain tissue. The KEGG pathway analysis showed significant differences in expression of genes involved in metabolic and immune pathways, such as the insulin signaling pathway, PI3K-Akt signaling pathway, cAMP signaling pathway, FoxO signaling pathway, AMPK signaling pathway, endocytosis, and apoptosis. Quantitative real-time PCR analysis confirmed that expression of the genes encoding the factors involved in those pathways differed between fasting and feeding fish. These results provide valuable information about the molecular response mechanism of black carp under fasting conditions.

The residue of simazine herbicide in the environment is known as one of pollutant stress for lizards by crippling its fitness on direct toxic effects and indirect food shortage via the food chain effects. Both stressors were considered in our experiment in the simazine exposure and food availability to lizards (Eremias argus). The results revealed that starvation significantly reduced the lizard\'s energy reserve and native immune function, while the accumulation of simazine in the liver was significantly increased. Simazine caused oxidative stress in the liver of lizards, but oxidative damage only occurred in the starved lizards. Simazine also changed the energy reserves, native immune function and detoxification of well-fed lizards, while the starved lizards showed different sensitivity to simazine. Simazine or starvation treatment independently activated the lizard HPA axis, but co-treatment caused the HPA axis inhibition. Besides, according to the variations on amino acid neurotransmitters, corticosterone hormone and thermoregulatory behavior, we inferred that lizards in threatens take the appropriate strategy on energy investment and allocation through neural, endocrine and behavioral pathways to maximize benefits in dilemma. Energy allocation was necessary, while suppression on any physiological process comes at a cost that is detrimental to long-term individual fitness.

Psychological stress can affect female reproduction by deteriorating oocyte quality, but the molecular mechanism is unclear. In this study, we used the chronic unpredictable stress model to study the effect of psychological stress on mouse oocyte competence during preimplantation stage, and RNA sequencing in single oocytes to analyze differential gene expression at the transcription level. Stress changed the serum levels of glucocorticoids and reduced oocyte developmental potential, depending on the strength of the stress. Strong stress (two stressors per day) reduced the fertilization rate and induced significant apoptosis in blastocysts. Moderate stress (one stressor per day) reduced the cleavage rate and blastocyst formation rate. Weak stress (one stressor every 2 days) did not have any significant negative effect on the fertilization, cleavage, and blastocyst formation. Hatching rate was not affected by stress, but stress retarded the development of the expanded blastocysts and inhibited the embryo development at early stages. Transcriptome analysis revealed that stress disturbed the expression of cell cycle regulators and apoptotic genes. The hub genes identified through protein-protein interaction analysis include Msln, Ceacam12, Psg16, Psg17, and Psg23, which are all carcinoembryonic or related genes involved in cell adhesion, proliferation, and migration. Thus, stress was inhibitory on fertilization and early embryo development in mice.

The aim of the research was to evaluate the dynamic changes of early posthatch starvation on residual yolk absorption, synthesis of macronutrients (protein, lipid, and glycogen), and organ development in broiler chicks. A total of 720 1-day-old chicks (Lingnan Yellow) were randomly assigned to 3 treatments: group A (nonfasted), group B (fasting for 24 h after placement), and group C (fasting for 48 h after placement). The trial lasted for 168 h, and water was provided ad libitum all the time. Sampling was performed at 0, 24, 48, 72, 120, and 168 h. Nonfasting (group A) promoted (P < 0.05) the absorption of amino acids, fatty acids, mineral elements, protein, and maternal antibody in the residual yolk of broiler chicks. The concentration of insulin-like growth factor 1 in plasma and the liver was higher (P < 0.05) in group A. Nonfasting enhanced (P < 0.05) the synthesis of protein and glycogen in the breast muscle and liver; the relative weights of the liver, pancreas, and spleen; and body weight, but retarded (P < 0.05) the synthesis of triglyceride in the liver. The results indicated that nonfasting (group A) after placement promoted the absorption of residual yolk and synthesis of protein and glycogen in the breast muscle and liver, whereas early feed deprivation promoted the synthesis of lipid in the liver. Thereby, nonfasting after placement promoted organ development and body growth of broiler chicks.