Prolonged Food Deprivation Research Articles

Role of serotonin in the lack of sensitization caused by prolonged food deprivation in Aplysia

Food deprivation may cause neurological dysfunctions including memory impairment. The mollusk Aplysia is a suitable animal model to study prolonged food deprivation-induced memory deficits because it can sustain up to 14 days of food deprivation (14DFD). Sensitization of defensive withdrawal reflexes has been used to illustrate the detrimental effects of 14DFD on memory formation. Under normal feeding conditions (i.e., two days food deprivation, 2DFD), aversive stimuli lead to serotonin (5-HT) release into the hemolymph and neuropil, which mediates sensitization and its cellular correlates including increased excitability of tail sensory neurons (TSNs). Recent studies found that 14DFD prevents both short-term and long-term sensitization, as well as short-term increased excitability of TSNs induced by in vitro aversive training. This study investigated the role of 5-HT in the absence of sensitization and TSN increased excitability under 14DFD. Because 5-HT is synthesized from tryptophan obtained through diet, and its exogeneous application alone induces sensitization and increases TSN excitability, we hypothesized that 1) 5-HT level may be reduced by 14DFD and 2) 5-HT may still induce sensitization and TSN increased excitability in 14DFD animals. Results revealed that 14DFD significantly decreased hemolymph 5-HT level, which may contribute to the lack of sensitization and its cellular correlates, while ganglia 5-HT level was not changed. 5-HT exogenous application induced sensitization in 14DFD Aplysia, albeit smaller than that in 2DFD animals, suggesting that this treatment can only induce partial sensitization in food deprived animals. Under 14DFD, 5-HT increased TSN excitability indistinguishable from that observed under 2DFD. Taken together, these findings characterize 5-HT metabolic deficiency under 14DFD, which may be compensated, at least in part, by 5-HT exogenous application.

Aestivation in Nature: Physiological Strategies and Evolutionary Adaptations in Hypometabolic States.

Aestivation is considered to be one of the "purest" hypometabolic states in nature, as it involves aerobic dormancy that can be induced and sustained without complex factors. Animals that undergo aestivation to protect themselves from environmental stressors such as high temperatures, droughts, and food shortages. However, this shift in body metabolism presents new challenges for survival, including oxidative stress upon awakening from aestivation, accumulation of toxic metabolites, changes in energy sources, adjustments to immune status, muscle atrophy due to prolonged immobility, and degeneration of internal organs due to prolonged food deprivation. In this review, we summarize the physiological and metabolic strategies, key regulatory factors, and networks utilized by aestivating animals to address the aforementioned components of aestivation. Furthermore, we present a comprehensive overview of the advancements made in aestivation research across major species, including amphibians, fish, reptiles, annelids, mollusks, and echinoderms, categorized according to their respective evolutionary positions. This approach offers a distinct perspective for comparative analysis, facilitating an understanding of the shared traits and unique features of aestivation across different groups of organisms.

Status of Expression of GnRH gene in Fed, Starved, and Refed Clarias Gariepinus (African Catfish)

Inadequate nutritional status impairs gonadal activities, which may induce reproductive difficulties in Clarias gariepinus. This research was aimed at evaluating the influence of starvation and subsequent refeeding on the expression of GnRH gene in Clarias gariepinus. One hundred and eighty (180) healthy juvenile Clarias gariepinus (African catfish) used in this study were randomly placed into two groups in triplicates. Fish in the control group were fed to satiation while fish in the treatment group were starved and refed and the fish in the control group were continuously fed. Brain tissue samples were collected after 7 days and 14 days of starvation, histopathology, and gene expression studies were done. The histological sections of brain tissue of week one starved and fed, C. gariepinus show neuronal cells on a background of neuropil while week two starved reveal badly distorted morphological architecture and degenerated neuronal cells. However, the week two re-fed, C. gariepinus brain tissue shows vacuolation of neuropil while the week two continuous fed shows no abnormalities. No mortality was recorded during starvation and the entire experimental period. In the second week of starvation, a decrease in the fold change (1.7) was observed when compared to week one while the fold change (1.2) observed in week three (week one of re-fed) is lower than the fold change observed in week one and two of starvation. The fold change (1.7) observed in week four (week two re-fed) is higher than the fold change observed in week three. The highest fold change (2.13) was observed in week one of starvation while the lowest fold change (1.24) was observed in week one of re-feeding. This study reveals that exposure of C. gariepinus to prolonged food deprivation alters the expression of GnRH, which might lead to impairment in the reproductive success of Clarias gariepinus.

Using an invertebrate model to investigate the mechanisms of short-term memory deficits induced by food deprivation

Although prolonged food deprivation is known to cause memory deficits, the underlying mechanisms are only partially understood. In this study, we began to investigate the cellular substrates of food deprivation-induced memory impairments in the invertebrate Aplysia. Following a single trial of noxious stimuli, Aplysia concurrently express short-term sensitization (an elementary form of learning in which withdrawal reflexes are enhanced) and short-term feeding suppression for at least 15 min. Cellular correlates of sensitization and feeding suppression include increased excitability of the tail sensory neurons (TSNs) controlling the withdrawal reflexes, and decreased excitability of feeding decision-making neuron B51, respectively. Recently, 14 days of food deprivation (14DFD) was reported to break the co-expression of sensitization and feeding suppression in Aplysia without health deterioration. Specifically, under 14DFD, sensitization was completely prevented while feeding suppression was present albeit attenuated. This study explored the cellular mechanisms underlying the absent sensitization and reduced feeding suppression under 14DFD. A reduced preparation was used to evaluate the short-term cellular modifications induced by delivering an aversive training protocol in vitro. TSN excitability failed to increase following in vitro training under 14DFD, suggesting that the lack of sensitization may be a consequence of the fact that TSN excitability failed to increase. B51 excitability also failed to decrease following in vitro training, indicating that additional neurons may contribute to the conserved albeit reduced feeding suppression in 14DFD animals. This study lays the foundations for the future use of the Aplysia model system to investigate the mechanisms underlying the memory impairments induced by prolonged food deprivation.

Elephant seal muscle cells adapt to sustained glucocorticoid exposure by shifting their metabolic phenotype.

Elephant seals experience natural periods of prolonged food deprivation while breeding, molting, and undergoing postnatal development. Prolonged food deprivation in elephant seals increases circulating glucocorticoids without inducing muscle atrophy, but the cellular mechanisms that allow elephant seals to cope with such conditions remain elusive. We generated a cellular model and conducted transcriptomic, metabolic, and morphological analyses to study how seal cells adapt to sustained glucocorticoid exposure. Seal muscle progenitor cells differentiate into contractile myotubes with a distinctive morphology, gene expression profile, and metabolic phenotype. Exposure to dexamethasone at three ascending concentrations for 48 h modulated the expression of six clusters of genes related to structural constituents of muscle and pathways associated with energy metabolism and cell survival. Knockdown of the glucocorticoid receptor (GR) and downstream expression analyses corroborated that GR mediates the observed effects. Dexamethasone also decreased cellular respiration, shifted the metabolic phenotype toward glycolysis, and induced mitochondrial fission and dissociation of mitochondria-endoplasmic reticulum (ER) interactions without decreasing cell viability. Knockdown of DNA damage-inducible transcript 4 (DDIT4), a GR target involved in the dissociation of mitochondria-ER membranes, recovered respiration and modulated antioxidant gene expression in myotubes treated with dexamethasone. These results show that adaptation to sustained glucocorticoid exposure in elephant seal myotubes involves a metabolic shift toward glycolysis, which is supported by alterations in mitochondrial morphology and a reduction in mitochondria-ER interactions, resulting in decreased respiration without compromising cell survival.

Effects of feeding condition on the morphology, behaviour and nutritional status of

Early life stages of migratory fish in rivers rely on physical transport mechanisms to carry them from spawning sites to distant nursery areas where they find food and refuge conditions. Starvation after a prolonged downriver drift could severely affect the colonisation and predator evasion capabilities of the larvae. In this study we investigated differences in the external morphology, nutritional condition and swimming abilities of fed and unfed Prochilodus lineatus early larvae under experimental conditions. After yolk reabsorption on Day 6, larvae were either fed with nauplii of Artemia salina or left unfed for up to 10 days. Larvae from each feeding regime (i.e. fed and unfed) were sampled daily from three aquaria, and the morphometry and routine swimming activity were determined and analysed together with a previously published RNA/DNA ratio dataset. The results were in agreement with previous investigations that indicated that the larvae of this species have starvation endurance; however, prolonged food deprivation is associated with a smaller body, anal depth and head length, as well as lower RNA/DNA ratios and reduced swimming ability.

Feeding state functionally reconfigures a sensory circuit to drive thermosensory behavioral plasticity.

Internal state alters sensory behaviors to optimize survival strategies. The neuronal mechanisms underlying hunger-dependent behavioral plasticity are not fully characterized. Here we show that feeding state alters C. elegans thermotaxis behavior by engaging a modulatory circuit whose activity gates the output of the core thermotaxis network. Feeding state does not alter the activity of the core thermotaxis circuit comprised of AFD thermosensory and AIY interneurons. Instead, prolonged food deprivation potentiates temperature responses in the AWC sensory neurons, which inhibit the postsynaptic AIA interneurons to override and disrupt AFD-driven thermotaxis behavior. Acute inhibition and activation of AWC and AIA, respectively, restores negative thermotaxis in starved animals. We find that state-dependent modulation of AWC-AIA temperature responses requires INS-1 insulin-like peptide signaling from the gut and DAF-16/FOXO function in AWC. Our results describe a mechanism by which functional reconfiguration of a sensory network via gut-brain signaling drives state-dependent behavioral flexibility.

D-Serine and d-Alanine Regulate Adaptive Foraging Behavior in Caenorhabditis elegans via the NMDA Receptor.

d-Serine (d-Ser) is a coagonist for NMDA-type glutamate receptors and is thus important for higher brain function. d-Ser is synthesized by serine racemase and degraded by d-amino acid oxidase. However, the significance of these enzymes and the relevant functions of d-amino acids remain unclear. Here, we show that in the nematode Caenorhabditis elegans, the serine racemase homolog SERR-1 and d-amino acid oxidase DAAO-1 control an adaptive foraging behavior. Similar to many organisms, C. elegans immediately initiates local search for food when transferred to a new environment. With prolonged food deprivation, the worms exhibit a long-range dispersal behavior as the adaptive foraging strategy. We found that serr-1 deletion mutants did not display this behavior, whereas daao-1 deletion mutants immediately engaged in long-range dispersal after food removal. A quantitative analysis of d-amino acids indicated that d-Ser and d-alanine (d-Ala) are both synthesized and suppressed during food deprivation. A behavioral pharmacological analysis showed that the long-range dispersal behavior requires NMDA receptor desensitization. Long-term pretreatment with d-Ala, as well as with an NMDA receptor agonist, expanded the area searched by wild-type worms immediately after food removal, whereas pretreatment with d-Ser did not. We propose that d-Ser and d-Ala are endogenous regulators that cooperatively induce the long-range dispersal behavior in C. elegans through actions on the NMDA receptor.SIGNIFICANCE STATEMENT In mammals, d-serine (d-Ser) functions as an important neuromodulator of the NMDA-type glutamate receptor, which regulates higher brain functions. In Caenorhabditis elegans, previous studies failed to clearly define the physiological significance of d-Ser, d-alanine (d-Ala), and their metabolic enzymes. In this study, we found that these d-amino acids and their associated enzymes are active during food deprivation, leading to an adaptive foraging behavior. We also found that this behavior involved NMDA receptor desensitization.

Effects of prolonged food limitation on energy metabolism and burrowing activity of an infaunal marine bivalve, Mya arenaria

Benthic organisms are subject to prolonged seasonal food limitation in the temperate shallow coastal waters that can cause energetic stress and affect their performance. Sediment-dwelling marine bivalves cope with prolonged food limitation by adjusting different physiological processes that might cause trade-offs between maintenance and other fitness-related functions. We investigated the effects of prolonged (42 days) food deprivation on bioenergetics, burrowing performance and amino acid profiles in a common marine bivalve, Mya arenaria collected in winter and spring. Food limitation of >15 days decreased respiration of the clams by 80%. Total tissue energy content was higher in spring-collected clams (reflecting higher lipid content) than in their winter counterparts. Prolonged food deprivation decreased the tissue energy content of clams, especially in winter. The levels of free amino acids transiently increased during the early phase of food deprivation possibly reflecting suppression of the protein synthesis or enhanced protein degradation. The levels of amino acids considered essential for bivalves were more tightly conserved than those of non-essential amino acids during starvation. The burrowing capacity of clams was negatively affected by food deprivation so that the time required for a burial cycle increased by 35–50% after 22–42 days of starvation. During the early phase of starvation, clams preferentially used lipids as fuel for burrowing, whereas carbohydrates were used at the later phase. These findings suggest that although M. arenaria can withstand prolonged food deprivation by lowering their basal maintenance costs and switching their fuel usage, their ecological functions (e.g. bioturbation and the energy transferable to the next trophic level) could be negatively impacted by starvation.

Functional Studies with Primary Cells Provide a System for Genome-to-Phenome Investigations in Marine Mammals.

Marine mammals exhibit some of the most dramatic physiological adaptations in their clade and offer unparalleled insights into the mechanisms driving convergent evolution on relatively short time scales. Some of these adaptations, such as extreme tolerance to hypoxia and prolonged food deprivation, are uncommon among most terrestrial mammals and challenge established metabolic principles of supply and demand balance. Non-targeted omics studies are starting to uncover the genetic foundations of such adaptations, but tools for testing functional significance in these animals are currently lacking. Cellular modeling with primary cells represents a powerful approach for elucidating the molecular etiology of physiological adaptation, a critical step in accelerating genome-to-phenome studies in organisms in which transgenesis is impossible (e.g., large-bodied, long-lived, fully aquatic, federally protected species). Gene perturbation studies in primary cells can directly evaluate whether specific mutations, gene loss, or duplication confer functional advantages such as hypoxia or stress tolerance in marine mammals. Here, we summarize how genetic and pharmacological manipulation approaches in primary cells have advanced mechanistic investigations in other non-traditional mammalian species, and highlight the need for such investigations in marine mammals. We also provide key considerations for isolating, culturing, and conducting experiments with marine mammal cells under conditions that mimic in vivo states. We propose that primary cell culture is a critical tool for conducting functional mechanistic studies (e.g., gene knockdown, over-expression, or editing) that can provide the missing link between genome- and organismal-level understanding of physiological adaptations in marine mammals.

Prolonged Fasting Increases DNA Methylation in Northern Elephant Seal Pups

Northern elephant seals (NES) are naturally exposed to extreme conditions, including prolonged food and water deprivation (fasting). NES pups initially nurse for a month before they are weaned and fast for two months. During this fasting period NES pups lose about 25% of their body mass, while maintaining biochemical homeostasis and supporting muscle development. The environment, especially stressful environmental conditions, can modify the methylation status of DNA, consequently regulating gene expression. We compared global DNA methylation between early (1–2 weeks) and late (7–8 weeks) fasting NES pups. DNA was extracted from white blood cells collected from fasting NES pups. Global DNA methylation was measured using a MethylFlash™ Global DNA Methylation (5‐mC) Kit. Prolonged fasting significantly increased global DNA methylation (p = 0.0463) in NES pups, suggesting a decrease in transcription activity. We are in the process of identifying changes in specific genes involved in growth, hypoxia tolerance, and metabolism between early and late fasting pups by analyzing the methylation status of CpG islands in putative promoter region sequences. Our initial results suggest that DNA methylation is an important regulator of gene expression during natural, prolonged food deprivation.

Determinants of undernutrition among children under-five years old in southern Ethiopia: does pregnancy intention matter? A community-based unmatched case-control study

BackgroundStunting, which describes a small height for one’s age, is an indicator of chronic malnutrition. It develops mainly as a result of prolonged food deprivation or a chronic disease or illness. Unintended pregnancies and unplanned births are among the psychological factors that negatively affect the nutritional status of children. Therefore, this study aimed to determine the effects of unintended pregnancies and other family and child characteristics on the nutritional status of children under 5 years old.MethodsA community-based unmatched case-control study was conducted among 302 children (151 cases and 151 controls) 6–59 months old in Wonago town, Gedeo Zone, Southern Ethiopia. The cases were stunted children and the controls were non-stunted children in the study area. The cases were randomly selected from among the stunted children, and the controls were randomly selected from among the non-stunted children. The descriptive characteristics of the respondents were compared using the chi-squared test, and a multivariable logistic regression was used to assess the effects of an unintended pregnancy on stunting, after controlling for the other variables, with a p value of 0.05.ResultsThe result revealed that unintended pregnancy is found to be among predictors of stunting where children from unintended pregnancy were about three times more likely to be stunted [AOR: 2.62, CI: (1.26, 5.45)]. The other predictors identified in this study were educational status of the father, wealth index of the household and daily meal frequency. From the finding, children from illiterate fathers [AOR: 3.43, CI: (1.04, 11.29)], children from poorer household economic status [AOR: 2.32, CI: (1.20, 4.49)] and children whom their daily meal frequency is below the recommended number of feeding [AOR: 4.50, CI: (1.31, 15.49)] were found to be more stunted.ConclusionsBased on the results of this study, the children born from unintended pregnancies exhibited a significantly higher risk of stunting. Therefore, preventing unintended pregnancy could play a great role in decreasing the risk of stunting in children.

Hepatic monoacylglycerol acyltransferase 1 is induced by prolonged food deprivation to modulate the hepatic fasting response

During prolonged fasting, the liver plays a central role in maintaining systemic energy homeostasis by producing glucose and ketones in processes fueled by oxidation of fatty acids liberated from adipose tissue. In mice, this is accompanied by transient hepatic accumulation of glycerolipids. We found that the hepatic expression of monoacylglycerol acyltransferase 1 (Mogat1), an enzyme with monoacylglycerol acyltransferase (MGAT) activity that produces diacyl-glycerol from monoacylglycerol, was significantly increased in the liver of fasted mice compared with mice given ad libitum access to food. Basal and fasting-induced expression of Mogat1 was markedly diminished in the liver of mice lacking the transcription factor PPARα. Suppressing Mogat1 expression in liver and adipose tissue with antisense oligonucleotides (ASOs) reduced hepatic MGAT activity and triglyceride content compared with fasted controls. Surprisingly, the expression of many other PPARα target genes and PPARα activity was also decreased in mice given Mogat1 ASOs. When mice treated with control or Mogat1 ASOs were gavaged with the PPARα ligand, WY-14643, and then fasted for 18 h, WY-14643 administration reversed the effects of Mogat1 ASOs on PPARα target gene expression and liver triglyceride content. In conclusion, Mogat1 is a fasting-induced PPARα target gene that may feed forward to regulate liver PPARα activity during food deprivation.

Mobilization of fat body glycogen and haemolymph trehalose under nutritional stress in Bombyx mori larvae in relation to their physiological age and the duration of food deprivation

In insects, fat body glycogen and haemolymph trehalose are principal carbohydrate reserves. Here, in Bombyx mori (Linnaeus, 1758), we report an accelerated fat body glycogen accumulation in feeding 5th instar larvae, when they reach the terminal growth period (TGP). Haemolymph trehalose and glucose levels, however, fluctuated between 7–21 mM and 0.8–10 mM, respectively, depending on the larval physiological age. Food deprivation triggered a dramatic increase in mobilization of glycogen in larvae at TGP than at active growth period (AGP), mobilized almost 78% of stored glycogen at an initial 12 h of food deprivation, possibly by increasing the percentage of active glycogen phosphorylase, as observed. This rapid glycogen mobilization, along with meeting the energy demand of starving tissues, might also have provided glucose for trehalose synthesis, as evident by observed hypertrehalosemia. A prolonged food deprivation (24–48 h) triggered hypotrehalosemia along with an increase in the enzyme activity of trehalase, and the transcript level of trehalase-2, indicating the utilization of trehalose as an energy source for the demanding tissues. Further, in TGP larvae, a prolonged food deprivation increased the level of haemolymph glucose (1.8–3.5 mM) as well as glucose/trehalose ratio, and this suggests that the fat body might have released the glucose molecules directly into the haemolymph, instead of utilizing it for trehalose synthesis, possibly to minimize the expenditure of energy. Thus, short-term food deprivation triggered an initial glycogen mobilization whereas, prolonged food deprivation led to the utilization of trehalose as an energy source. Hence, mobilization of carbohydrate reserves varied depending on the larval physiological age and the extent of food deprivation period. The future investigation can expand our understanding on the role of glucose as an important haemolymph sugar along with trehalose.

Proteomics Analysis Reveals the Implications of Cytoskeleton and Mitochondria in the Response of the Rat Brain to Starvation.

Long-term starvation provokes a metabolic response in the brain to adapt to the lack of nutrient intake and to maintain the physiology of this organ. Here, we study the changes in the global proteomic profile of the rat brain after a seven-day period of food deprivation, to further our understanding of the biochemical and cellular mechanisms underlying the situations without food. We have used two-dimensional electrophoresis followed by mass spectrometry (2D-MS) in order to identify proteins differentially expressed during prolonged food deprivation. After the comparison of the protein profiles, 22 brain proteins were found with altered expression. Analysis by peptide mass fingerprinting and MS/MS (matrix-assisted laser desorption-ionization-time of flight mass spectrometer, MALDI-TOF/TOF) enabled the identification of 14 proteins differentially expressed that were divided into 3 categories: (1) energy catabolism and mitochondrial proteins; (2) chaperone proteins; and (3) cytoskeleton, exocytosis, and calcium. Changes in the expression of six proteins, identified by the 2D-MS proteomics procedure, were corroborated by a nanoliquid chromatography-mass spectrometry proteomics procedure (nLC-MS). Our results show that long-term starvation compromises essential functions of the brain related with energetic metabolism, synapsis, and the transmission of nervous impulse.

Not the Function of Eating, but Spontaneous Activity and Energy Expenditure, Reflected in "Restlessness" and a "Drive for Activity" Appear to Be Dysregulated in Anorexia Nervosa: Treatment Implications.

Anorexia nervosa (AN) is uncommon as a syndrome, despite widespread dieting or voluntary food restriction, especially among female adolescents. This suggests that restriction of caloric intake might not be the only component driving weight loss in AN. Historical observations and experimental evidence from energy expenditure studies and recordings from movement sensors reviewed in this paper reveal that AN is associated with motor activity levels and with an energy output not significantly different from that in normal-weight healthy age-matched controls. By contrast, other conditions of prolonged caloric under-nutrition are typically associated with loss of energy, slowing of movements and a decrease in self-initiated activity and well-being. Several hypotheses can be inferred from the findings: (a) that long term severe caloric restriction fails in downregulating movements and energy expenditure in AN. (b) Clinically and subjectively observable as mental and physical restlessness and continued motor activity, this restless energy, differing in intensity, seems to serve as the permissive factor for and possibly to drive exercise and hyperactivity in AN. (c) Such restless energy and increased arousal, generated sometime in the course of the weight loss process, appear to enhance the person’s self-perception and wellbeing, to heighten proprioception, to intensify body awareness and to improve self-esteem. (d) Restlessness and continued motor activity may constitute a phenotype of AN. The therapeutic value of the concept of an abnormality in the energy regulatory system, likely the result of a host of genetic and epigenetic changes in AN, lies primarily in its heuristic and explanatory power and its potential for disease prevention. Restless energy as a permissive and important component for the development and in the maintenance of AN, does not fundamentally alter treatment, since prolonged food deprivation is the principal causal factor for the development of AN. Re-nutrition within a structured treatment plan, to include individual and family therapy and, if indicated, heat application, remains the most effective symptomatic treatment for AN. Corroboration of the concept of restless activation will require the patient’s cooperation and input to identify and capture more precisely the experiences, sensations, and changes that allow the emaciated patient to remain mobile and active.

Effects of internal and external factors on the budgeting between defensive and non-defensive responses in Aplysia

Following exposure to aversive stimuli, organisms budget their behaviors by augmenting defensive responses and reducing/suppressing non-defensive behaviors. This budgeting process must be flexible to accommodate modifications in the animal’s internal and/or external state that require the normal balance between defensive and non-defensive behaviors to be adjusted. When exposed to aversive stimuli, the mollusk Aplysia budgets its behaviors by concurrently enhancing defensive withdrawal reflexes (an elementary form of learning known as sensitization) and suppressing feeding. Sensitization and feeding suppression are consistently co-expressed following different training protocols and share common temporal domains, suggesting that they are interlocked. In this study, we attempted to uncouple the co-expression of sensitization and feeding suppression using: 1) manipulation of the animal’s motivational state through prolonged food deprivation and 2) extended training with aversive stimuli that induces sensitization lasting for weeks. Both manipulations uncoupled the co-expression of the above behavioral changes. Prolonged food deprivation prevented the expression of sensitization, but not of feeding suppression. Following the extended training, sensitization and feeding suppression were co-expressed only for a limited time (i.e., 24 h), after which feeding returned to baseline levels as sensitization persisted for up to seven days. These findings indicate that sensitization and feeding suppression are not interlocked and that their co-expression can be uncoupled by internal (prolonged food deprivation) and external (extended aversive training) factors. The different strategies, by which the co-expression of sensitization and feeding suppression was altered, provide an example of how budgeting strategies triggered by an identical aversive experience can vary depending on the state of the organism.

Increased sensitivity of thyroid hormone-mediated signaling despite prolonged fasting

Thyroid hormones (TH) can increase cellular metabolism. Food deprivation in mammals is typically associated with reduced thyroid gland responsiveness, in an effort to suppress cellular metabolism and abate starvation. However, in prolonged-fasted, elephant seal pups, cellular TH-mediated proteins are up-regulated and TH levels are maintained with fasting duration. The function and contribution of the thyroid gland to this apparent paradox is unknown and physiologically perplexing. Here we show that the thyroid gland remains responsive during prolonged food deprivation, and that its function and production of TH increase with fasting duration in elephant seals. We discovered that our modeled plasma TH data in response to exogenous thyroid stimulating hormone predicted cellular signaling, which was corroborated independently by the enzyme expression data. The data suggest that the regulation and function of the thyroid gland in the northern elephant seal is atypical for a fasted animal, and can be better described as, “adaptive fasting”. Furthermore, the modeling data help substantiate the in vivo responses measured, providing unique insight on hormone clearance, production rates, and thyroid gland responsiveness. Because these unique endocrine responses occur simultaneously with a nearly strict reliance on the oxidation of lipid, these findings provide an intriguing model to better understand the TH-mediated reliance on lipid metabolism that is not otherwise present in morbidly obese humans. When coupled with cellular, tissue-specific responses, these data provide a more integrated assessment of thyroidal status that can be extrapolated for many fasting/food deprived mammals.

Gene Network and Adipose Transcriptome Analysis of the Northern Elephant Seal During Prolonged Food Deprivation

Many animals have been extensively studied for their potential to elucidate cellular pathways that can lead to breakthroughs or progress in the development of therapeutic strategies against human diseases such as cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus. The northern elephant seal (Mirounga angustirostris) is a natural model for these and other maladies, and its extraordinary physiology has been the subject of substantial examination since their return from the brink of extinction. The most notable contributions have come from the assessment of endocrine changes in peripheral tissues, including adipose and muscle. Yet, the reference sequence for adipose, has not yet been described. Here, we present the first adipose‐derived northern elephant seal transcriptome assembly in response to fasting with RNA from two separate fasting phases. In this de novo assembly, differential expression analysis between fasting periods demonstrated the upregulation of a large number of metabolism‐driving transcripts. This data will provide and serve as a tool in the necessary continuation of future studies elucidating the unique physiology of the northern elephant seal.

Socio-economic and demographic correlates of stunting among adolescents of Assam, North-east India

The prevalence of stunting (low height-for-age) is a key indicator of long-term chronic undernutrition which reflects an anthropometric failure to reach linear growth potentials due to prolonged food deprivation and/or disease or illness during the early stage of life. The present study assesses the prevalence and socio-economic and demographic correlates of stunting among adolescents of the North-east India. This cross-sectional study was undertaken among 1,818 (830 boys; 988 girls) adolescents (aged 10-18 years) belonging to ethnically heterogeneous populations of Karbi Anglong district of Assam, using stratified random sampling method. Anthropometric measurements of height and weight were recorded using standard procedures. Socio-economic and demographic variables were obtained using pre-structured schedule. The age-sex specific L, M and S reference values were used to calculate height-for-age Z-score (HAZ). According to WHO, HAZ found to be <−2SD was classified as stunting. The data were analysed using descriptive statistics, t-test, ANOVA, chi-square analyses, binary and step-wise multiple logistic regression analysis in SPSS (version, 17.0). The prevalence of stunting was observed to be significantly higher among boys (48.4%) than girls (37.8%) (p<0.01). Age-sex specific prevalence was found to be higher among boys than girls aged 14-18 years and contrary were observed among girls aged 10-14 years (p>0.05). The binary logistic regression analysis showed that several socio-economic and demographic variables were significantly associated with stunting (p<0.05). The step-wise multiple logistic regression analysis showed that sex (boys), age groups (13-15 years and 16-18 years), father’s occupation (cultivator) and Rupees ≤5000 household income was significantly associated with stunting (p<0.05). Appropriate nutritional intervention programmes and dissemination of knowledge at population level related to undernutrition are necessary to ameliorate their nutritional status.