Maintenance Of Energy Balance Research Articles

BIOCHEMICAL INDICATORS OF MILITARY BLOOD ON THE ISCHEMIC AND DENERVATION PROCESS IN MUSCLES AFTER A MINE-EXPLOSIVE INJURYS

The injuries received are accompanied by massive damage to the soft tissues of the limbs, main vessels and nerves, and the development of compartment syndrome. Violation of muscle function in the case of a limb injury can be both a consequence of denervation — as a result of damage to peripheral nerves, and ischemia with subsequent necrosis and fibrosis — as a result of direct or indirect damage to muscles, «tenotomy syndrome» — in case of traumatic damage to tendons and muscles yams, with the simultaneous combination of denervation and ischemia. Markers for assessing the state of muscle tissue — levels of Na+, K+ and Ca++ electrolytes, indicators of kidney function (urea, creatinine); glucose and the products of its transformations — lactate (lacticacid) and pyruvate (pyruvic acid) and, finally, muscle enzymes, namely creatine kinase (CK) and lactate dehydrogenase (LDH). Objective. To study the biochemical indicators of blood (activity of energy metabolism enzymes and electrolyte content) of military personnel with ischemic contracture and muscle denervation after a mine-explosive injury. Methods. The blood serum of 45 people, who were divided into IV groups, was analyzed. The average age of patients of the II group was 33.75 ± 3.46; III — 37 ± 3.66; IV — 35.86 ± 2.35. The results. The activity of LDH and CK and the content of electrolytes Na+, K+, Ca++ were determined in blood serum. Conclusions. LDH plays a key role in lactate metabolism and maintenance of energy balance in skeletal muscle. Its increased activity indicates the presence of hypoxia due to ischemic contracture of the limb and damage to peripheral nerves. KK enzyme protects cell membranes from damage. The tendency to decrease the activity of CC is a negative sign that reflects the initial process of destruction of the cell membranes of muscles damaged by a mine-explosive injury. The obtained results can be used to determine the severity of pathological processes in patients after traumatic damage to peripheral nerves and ischemic contracture, as well as when assessing the expediency of surgical intervention.

Dysfunction of the adhesion G protein-coupled receptor latrophilin 1 (ADGRL1/LPHN1) increases the risk of obesity

Obesity is one of the diseases with severe health consequences and rapidly increasing worldwide prevalence. Understanding the complex network of food intake and energy balance regulation is an essential prerequisite for pharmacological intervention with obesity. G protein-coupled receptors (GPCRs) are among the main modulators of metabolism and energy balance. They, for instance, regulate appetite and satiety in certain hypothalamic neurons, as well as glucose and lipid metabolism and hormone secretion from adipocytes. Mutations in some GPCRs, such as the melanocortin receptor type 4 (MC4R), have been associated with early-onset obesity. Here, we identified the adhesion GPCR latrophilin 1 (ADGRL1/LPHN1) as a member of the regulating network governing food intake and the maintenance of energy balance. Deficiency of the highly conserved receptor in mice results in increased food consumption and severe obesity, accompanied by dysregulation of glucose homeostasis. Consistently, we identified a partially inactivating mutation in human ADGRL1/LPHN1 in a patient suffering from obesity. Therefore, we propose that LPHN1 dysfunction is a risk factor for obesity development.

The potential role of creatine supplementation in neurodegenerative diseases.

The maintenance of energy balance in the body, especially in energy-demanding tissues like the muscles and the central nervous system, depends on creatine (Cr). In addition to improving muscle function, Cr is necessary for the bioenergetics of the central nervous system because it replenishes adenosine triphosphate without needing oxygen. Furthermore, Cr possesses anti-oxidant, anti-apoptotic, and anti-excitotoxic properties. Clinical research on neurodegenerative illnesses has shown that Cr supplementation results in less effective outcomes. With a brief update on the possible role of Cr in human, animal, and in vitro experiments, this review seeks to offer insights into the ideal dosage regimen. Using specified search phrases, such as "creatine and neurological disorder," "creatine supplementation and neurodegenerative disorders," and "creatine and brain," we searched articles in the PubMed database and Google Scholar. We investigated the association between creatine supplementation and neurodegenerative illnesses by examining references. The neuroprotective effects of Cr were observed in in vitro and animal models of certain neurodegenerative diseases, while clinical trials failed to reproduce favorable outcomes. Determining the optimal creatinine regime for increasing brain creatinine levels is essential for maintaining brain health and treating neurodegeneration.

Energy Regulation in Inflammatory Sarcopenia by the Purinergic System

The purinergic system has a dual role: the maintenance of energy balance and signaling within cells. Adenosine and adenosine triphosphate (ATP) are essential for maintaining these functions. Sarcopenia is characterized by alterations in the control of energy and signaling in favor of catabolic pathways. This review details the association between the purinergic system and muscle and adipose tissue homeostasis, discussing recent findings in the involvement of purinergic receptors in muscle wasting and advances in the use of the purinergic system as a novel therapeutic target in the management of sarcopenia.

An Overview of Appetite Regulation Mechanisms

Maintaining body weight is momentous in quality of life. Appetite takes an important role in establishing the balance of daily food absorption and spent energy and, accordingly, controlling body weight. There is a complex physiological control regulation in the maintenance of energy balance. The regulation of appetite is carried out by central and peripheral signals. The hypothalamus, brainstem, and reward centers, which are involved in central regulation, provide management of food absorption by integrating signals from the peripheral. Gastrointestinal hormones in the peripheral system regulate the digestion and absorption of nutrients. In the central nervous system, these hormones act as neurotransmitters. The ability to adjust food absorption in response to changes in energy status is an essential component of maintaining energy homeostasis. In cases where energy homeostasis cannot be balanced, it risks human life and causes a decrease in their quality of life. Diseases such as anorexia, which is characterized by low body weight, or obesity, which is characterized by increased body weight, may occur. A full understanding of the mechanism of appetite may offer new treatment opportunities in the elimination of diseases and complications that may develop due to these diseases. In this context, central and peripheral processes in the adjustment of food intake were reviewed in our study.

Adiponectin affects uterine steroidogenesis during early pregnancy and the oestrous cycle: An in vitro study

Reproduction in females is an energetically demanding process. We assumed that adiponectin (ADPN), known for its role in energy balance maintenance, is also engaged in the regulation of uterine steroidogenesis in the pig. We determined the impact of ADPN alone or in combination with insulin (INS) on testosterone (T), estrone (E1) and estradiol (E2) secretion by porcine endometrium and myometrium, uterine expression of CYP17A1 and CYP19A3 genes, and endometrial abundance of P450C17 and P450AROM proteins during the peri-implantation period and the oestrous cycle, using radioimmunoassay, qPCR, and Western Blot, respectively. During pregnancy, in the endometrial explants from days 10–11, ADPN decreased CYP17A1 gene expression, P450C17 protein abundance and T secretion, whereas increased E1 secretion. On days 12–13 of pregnancy, ADPN decreased CYP17A1 and CYP19A3 expression, P450C17 and P450AROM protein abundance and E1 secretion, but stimulated T secretion. On days 15–16 of pregnancy, ADPN decreased P450C17 protein accumulation but enhanced CYP19A3 expression and E1 secretion. On days 27–28 of pregnancy, ADPN increased CYP17A1 and CYP19A3 mRNA content and T secretion in this tissue and decreased P450C17 content. ADPN effect on myometrial explants was dependent on stage of gestation or oestrous cycle. Moreover, INS treatment modulated basal and ADPN-affected steroidogenic enzymes gene and protein expression and steroids secretion. The results obtained indicate that ADPN may affect processes required for successful implantation such as steroidogenesis. ADPN and INS were also shown to modulate each other action, which indicates that the proper course of uterine steroidogenesis may be dependent on both hormones’ interaction.

HIF3A Inhibition Triggers Browning of White Adipocytes via Metabolic Rewiring.

Maintenance of energy balance between intake and expenditure is a prerequisite of human health, disrupted in severe metabolic diseases, such as obesity and type 2 diabetes (T2D), mainly due to accumulation of white adipose tissue (WAT). WAT undergoes a morphological and energetic remodelling toward brown adipose tissue (BAT) and the BAT activation has anti-obesity potential. The mechanisms or the regulatory factors able to activate BAT thermogenesis have been only partially deciphered. Identifying novel regulators of BAT induction is a question of great importance for fighting obesity and T2D. Here, we evaluated the role of Hif3α in murine pre-adipocyte 3T3-L1 cell line, a versatile and well characterized biological model of adipogenesis, by gain- and loss-of function approaches and in thermogenesis-induced model in vivo. HIF3A is regulated by inflammation, it modulates lypolysis in adipose tissue of obese adults, but its role in energy metabolism has not previously been investigated. We characterized gene and protein expression patterns of adipogenesis and metabolic activity in vitro and mechanistically in vivo. Overexpression of Hif3α in differentiating adipocytes increases white fat cells, whereas silencing of Hif3α promotes “browning” of white cells, activating thermogenesis through upregulation of Ucp1, Elovl3, Prdm16, Dio2 and Ppargc1a genes. Investigating cell metabolism, Seahorse Real-Time Cell Metabolism Analysis showed that silencing of Hif3α resulted in a significant increase of mitochondrial uncoupling with a concomitant increase in acetyl-CoA metabolism and Sirt1 and Sirt3 expression. The causal Hif3α/Ucp1 inverse relation has been validated in Cannabinoid receptor 1 (CB1) knockout, a thermogenesis-induced model in vivo. Our data indicate that Hif3α inhibition triggers “browning” of white adipocytes activating the beneficial thermogenesis rewiring energy metabolism in vitro and in vivo. HIF3A is a novel player that controls the energy metabolism with potential applications in developing therapy to fight metabolic disorders, as obesity, T2D and ultimately cancer.

The Pleiotropic Potential of BDNF beyond Neurons: Implication for a Healthy Mind in a Healthy Body.

Brain-derived neurotrophic factor (BDNF) represents one of the most widely studied neurotrophins because of the many mechanisms in which it is involved. Among these, a growing body of evidence indicates BDNF as a pleiotropic signaling molecule and unveils non-negligible implications in the regulation of energy balance. BDNF and its receptor are extensively expressed in the hypothalamus, regions where peripheral signals, associated with feeding control and metabolism activation, and are integrated to elaborate anorexigenic and orexigenic effects. Thus, BDNF coordinates adaptive responses to fluctuations in energy intake and expenditure, connecting the central nervous system with peripheral tissues, including muscle, liver, and the adipose tissue in a complex operational network. This review discusses the latest literature dealing with the involvement of BDNF in the maintenance of energy balance. We have focused on the physiological and molecular mechanisms by which BDNF: (I) controls the mitochondrial function and dynamics; (II) influences thermogenesis and tissue differentiation; (III) mediates the effects of exercise on cognitive functions; and (IV) modulates insulin sensitivity and glucose transport at the cellular level. Deepening the understanding of the mechanisms exploited to maintain energy homeostasis will lay the groundwork for the development of novel therapeutical approaches to help people to maintain a healthy mind in a healthy body.

Relationship between Energy Balance and Circulating Levels of Hepcidin and Ferritin in the Fasted and Postprandial States.

Markers of iron metabolism are altered in new-onset diabetes, but their relationship with metabolic signals involved in the maintenance of energy balance is poorly understood. The primary aim was to explore the associations between markers of iron metabolism (hepcidin and ferritin) and markers of energy balance (leptin, ghrelin, and the leptin/ghrelin ratio) in both the fasted and postprandial states. These associations were also studied in the sub-groups stratified by diabetes status. This was a cross-sectional study of individuals without disorders of iron metabolism who were investigated after an overnight fast and, in addition, some of these individuals underwent a mixed meal test to determine postprandial responses of metabolic signals. The associations between hepcidin, ferritin, and leptin, ghrelin, leptin/ghrelin ratio were studied using several multiple linear regression models. A total of 76 individuals in the fasted state and 34 individuals in the postprandial state were included. In the overall cohort, hepcidin was significantly inversely associated with leptin (in the most adjusted model, the β coefficient ± SE was −883.45 ± 400.94; p = 0.031) and the leptin/ghrelin ratio (in the most adjusted model, the β coefficient ± SE was −148.26 ± 61.20; p = 0.018) in the fasted state. The same associations were not statistically significant in the postprandial state. In individuals with new-onset prediabetes or diabetes (but not in those with normoglycaemia or longstanding prediabetes or diabetes), hepcidin was significantly inversely associated with leptin (in the most adjusted model, the β coefficient ± SE was −806.09 ± 395.44; p = 0.050) and the leptin/ghrelin ratio (in the most adjusted model, the β coefficient ± SE was −129.40 ± 59.14; p = 0.037). Leptin appears to be a mediator in the link between iron metabolism and new-onset diabetes mellitus. These findings add to the growing understanding of mechanisms underlying the derangements of glucose metabolism.

Dietary Protein From Different Sources Exerted a Great Impact on Lipid Metabolism and Mitochondrial Oxidative Phosphorylation in Rat Liver.

Associations between meat diets and human health have been widely considered. In this study, we focused on long-term effects of different sources of meat protein on liver metabolic enzymes. For 90 days, rats were fed with semisynthetic diets that differed only with protein source. Casein was used as a reference and isolated soybean, fish, chicken, pork, and beef proteins were compared. Changes in liver proteome were determined by isobaric tag for relative and absolute quantitation (iTRAQ) labeling and liquid chromatography electrospray ionization tandem mass spectrometry/mass spectrometry (LC–ESI–MS/MS). Fish and pork protein diets upregulated the gene expression involved in cholesterol synthesis and esterification, and pork protein diet also upregulated the gene expression of high-density lipoprotein receptor and low-density lipoprotein receptor. Chicken, pork, and beef protein diets upregulated the gene expression involved in cholesterol reverse transport and bile acid production, which increased the total cholesterol level in the fish protein diet group. Total cholesterol levels in liver were lower in the pork and beef protein diet groups. Triglyceride levels in liver were lower in chicken, pork, and beef protein diet groups. Peroxisomal proliferator-activated receptor-gamma coactivator-1 was upregulated by chicken, pork and beef protein diets, and promoted the degradation and metabolism of triglyceride, resulting in lower triglyceride in the three diet groups. Meat proteins at a recommended level could be more conducive to cholesterol degradation, triglyceride decomposition, and energy balance maintenance at a healthy level. The findings give a new insight into the associations between meat diet intake and human health.

THE NUTRISS STUDY: A NEW APPROACH TO CALIBRATE DIET AND EXERCISE IN LONG-TERM SPACE MISSIONS

Energy balance maintenance is crucial to preserve astronaut's wellness during longduration-spaceflight. Nutritional intervention can counteract the detrimental effect of microgravity on body composition and metabolism. NutrISS is an Italian Space Agency biomedical experiment. This proof-of-concept study aim to monitor the body composition of astronauts and to provide nutritional advice during long-term mission. The study has been executed on the ISS and sponsored by ESA. The payloads selected for the mission “BEYOND” result from a public-call funded and coordinated by ASI, in the frame of its national mission of promoting and fostering the culture of space across the Country and providing access to the ISS as a laboratory in space to the Italian research community. The utilization support services is ensured by Argotec/Telespazio (UTISS Team). The Italian astronaut Luca Parmitano underwent to baseline data collections, i.e. body composition, anthropometric evaluation and energy and metabolic assessment carried out by the scientific team. Body composition has been assessed by a BioImpedance Analyser device (Akern) modified by Kayser Italia. To maintain the near-neutral energy balance, the NutISS team monitored monthly the astronaut body mass during flight. Results are now classified for privacy reasons. The study was extended since collected data improved physical performance and quality of life of the astronaut during spaceflight and optimize the astronaut recovery-phases on Earth after landing. Obtained experimental data could have an important impact both on astronaut quality of life and clinical management of malnourished and/or obese immobilized patients, therefore improving the quality of human bedridden patients on Earth.

Leptin signalling in teleost fish with emphasis in food intake regulation

Leptin, the product of the obese (ob or Lep) gene, was first cloned in teleost fish in 2005, more than a decade after its identification in mammals. This was because bony fish and mammalian leptins share a very low amino acid sequence identity, which suggests different functionality of the leptin system in fish compared to that of mammals. Indeed, major differences are evident between the mammalian and fish leptin system. Thus, for instance, mammalian leptin is synthesized and released by the adipose tissue in response to the amount of fat depots, while several tissues (mainly the liver) are the main sources of leptin in fish, whose determining factors of production are still unclear. In mammals, the main physiological role for leptin is its involvement in the maintenance of energy balance by decreasing food intake and increasing energy expenditure, although a wide variety of actions have been attributed to this hormone (e.g., regulation of lipid and carbohydrate metabolism, reproduction and immune functions). In fish, available literature also points towards a multifunctional nature for leptin, although knowledge on its functions is limited. In this review, we offer an overview of teleostean leptin structure and mechanism of action, and discuss the available knowledge on the role of this hormone in food intake regulation in teleost fish, aiming to provide a comparative overview between the functioning of the teleostean and mammalian leptin systems.

The Nutriss Study: A New Approach to Calibrate Diet and Exercise in Long-Term Space Missions to Maintain Body Fat, Muscle and Fluid Homeostasis

Energy balance maintenance is crucial to preserve astronaut’s wellness and quality of life during long-duration spaceflight and nutritional intervention can effectively counteract the detrimental effect of microgravity on skeletal muscle mass and metabolism. NutrISS (Nutrition monitoring for the International Space Station) is an Italian Space Agency (ASI) biomedical experiment investigating the changes in body composition during long-term spaceflight. The goal of this proof-of-concept study is to monitor the body composition of astronauts and, if needed, to provide nutritional advice during the mission. It has been executed on the ISS, from July 2019 till January 2020 and sponsored by ESA. The payloads selected for the mission “BEYOND” result from a public-call funded and coordinated by ASI, in the frame of its national mission of promoting and fostering the culture of space across the Country and providing access to the ISS as a laboratory in space to the Italian research community. The utilization support services is ensured by Argotec/Telespazio (UTISS Team). An astronaut underwent to baseline data collections, i.e. body composition, anthropometric evaluation and energy and metabolic assessment carried out by the scientific team. Body composition, estimated through resistance/reactance to a low-intensity current has been assessed with a Bio-Impedance Analyser (BIA) device manufactured by Akern and modified by Kayser Italia. To maintain the participant in near-neutral energy balance, the science team monitored monthly the astronaut body mass during the entire space flight period. Advice on energy intake was given to the astronaut when needed.

The re-emergence of adipose innervation as a research focus.

In the pursuit of understanding metabolic control and energy balance, peripheral nerve communication between adipose tissues and the brain has been largely ignored. This Comment discusses the need for additional research that focuses on the role of adipose peripheral nerve function in the maintenance of energy balance.

Metabolic hormones and the regulation of spermatogenesis in fishes

Metabolic hormones play essential regulatory roles in many biological processes, including morphogenesis, growth, and reproduction through the maintenance of energy balance. Various metabolic hormones originally discovered in mammals, including ghrelin, leptin, and nesfatin-1 have been identified and characterized in fish. However, physiological roles of these metabolic hormones in regulating reproduction are largely unknown in fishes, especially in males. While the information available is restricted, this review attempts to summarize the main findings on the roles of metabolic peptides on the reproductive system in male fishes with an emphasis on testicular development and spermatogenesis. Specifically, the primary goal is to review the physiological interactions between hormones that regulate reproduction and hormones that regulate metabolism as a critical determinant of testicular function. A brief introduction to the localization of metabolic hormones in fish testis is also provided. Besides, the consequences of fasting and food deprivation on testicular development and sperm quality will be discussed with a focus on interactions between metabolic and reproductive hormones.

AMPK-Targeted Effector Networks in Mycobacterial Infection.

AMP-activated protein kinase (AMPK), a key metabolic regulator, plays an essential role in the maintenance of energy balance in response to stress. Tuberculosis (TB), primarily caused by the pathogen Mycobacterium tuberculosis (Mtb), remains one of the most important infectious diseases worldwide, characterized by both high incidence and mortality. Development of new preventive and therapeutic strategies against TB requires a profound understanding of the various host-pathogen interactions that occur during infection. Emerging data suggest that AMPK plays an essential regulatory role in host autophagy, mitochondrial biogenesis, metabolic reprogramming, fatty acid β-oxidation, and the control of pathologic inflammation in macrophages during Mtb infection. As described in this review, recent studies have begun to define the functional properties of AMPK modulators capable of restricting intracellular bacteria and promoting host defenses. Several host defense factors in the context of AMPK activation also participate in autophagic and non-autophagic pathways in a coordinated manner to enhance antimicrobial responses against Mtb infection. A better understanding of these AMPK-targeted effector networks offers significant potential for the development of novel therapeutics for human TB and other infectious diseases.

The relationship between hourly energy balance and fat mass in female collegiate soccer players

Introduction: Soccer athletes have better performance if they maintain low fat mass (FM) relative to fat-free mass. Recent evidence suggests that maintenance of energy balance (EB) is associated with lower FM in athletes. Prior studies have used daily EB rather than hourly, but this approach does not consider duration of time athletes spend in EB versus surplus or deficit. Objective: Test the hypotheses that (1) time spent in EB is inversely associated with FM, and (2) athletes with mean hourly EB in the deficit range have lower FM than those in balance or surplus. Methods: Collegiate female soccer players (n = 20) were enrolled in this cross-sectional study. A 3-day diet/activity record was obtained and analysed to estimate EB in hourly increments. Hourly EB was categorized as: Surplus, > 400 kcal EB; Balance, between ± 400 kcal EB; Deficit, < -400 kcal EB. Total hours spent in each category and mean EB (kcals) was calculated from the 3-day period. Bioelectrical Impedance Analysis was used to derive indices of FM (total FM in kg, % fat, fat mass index). Pearson correlations evaluated associations between FM measures and time spent in each EB category. One-way ANOVA with Tukey post-hoc testing was used to assess differences in FM among athletes stratified into surplus, balance, or deficit based on mean hourly EB. Results: Hourly energy deficit was associated with higher FM compared to energy surplus or balance. Conclusion: Female collegiate soccer players who sustain EB during the day, and limit time spent in energy deficit, had lower FM measures.

Hypothalamic AgRP neurons and the regulation of appetite and body weight: A review

The maintenance of energy balance is essential for the survival of animals. The hypothalamus in the brain plays a central role in this process through the integration of neural, nutritional and hormonal signals. Multiple and distributed neuronal populations in the hypothalamus form complex circuits to regulate appetite and body weight. Located in the arcuate nucleus of hypothalamus, agouti-related peptide (AgRP)-expressing cells are known as the hunger-promoting neurons. Over the past three decades, extensive studies have been performed to understand the role of AgRP neurons in energy balance control. AgRP neurons are both necessary and sufficient to orchestrate feeding behavior. The AgRP neuron activity adapts to and thereby is regulated by the nutritional status in the body. Furthermore, we now know that this alternation is driven by various circulating hormones, such as Leptin and Ghrelin, as well as synaptic inputs from upstream neurons. Neurotransmitters (e.g. glutamate and GABA) play a vital role in the regulation of AgRP neuron activity. The excitatory glutamatergic input is required in fasting-related activation of AgRP neurons, whereas the inhibitory GABAergic inputs is crucial in the rapid reduction of AgRP neuron activity in response to food-related cues, and thus, to terminate a meal. In addition to these molecules, signaling molecules and pathways in AgRP neurons, such as receptors, ion channels, kinases (e.g. IKKβ), endoplasmic reticulum stress (ER stress) and mitochondrial dynamic, are critically involved in the control of its activity. Moreover, AgRP neurons release neuropeptides AgRP and NPY, as well as neurotransmitter GABA to regulate neuronal activity. Both AgRP and NPY potently promote appetite. Although NPY is widely expressed in the central nervous system, it is mainly co-expressed with AgRP in the arcuate nucleus of hypothalamus. The appetite-promoting effect of NPY is mediated by Y1 and Y5 receptors, while AgRP exert its orexigenic effect mainly by antagonizing the central melanocortin system. Surprisingly, ablation of AgRP neurons in neonates has little effect on body weight, whereas these neurons are essential for the maintenance of appetite in adult mice. Moreover, accumulating evidences indicate that GABA released by AgRP neurons is required to retain animals appetite. At the circuit level, AgRP neurons project to both intra- and extra-hypothalamic regions to regulate energy balance. For example, in arcuate nucleus, AgRP neurons innervate and inhibit POMC neurons via the inhibitory GABAergic synapses. Conversely, POMC neurons release β-endorphin, a μ-opioid receptor agonist, to inhibit the activity of AgRP neurons. In summary, AgRP neurons play a crucial role in the regulation of appetite and energy balance. Targeting hypothalamic AgRP neurons might be a relevant approach to treat common obesity.

Alterations of pigment composition and their interactions in response to different light conditions in the diatom Chaetoceros gracilis probed by time-resolved fluorescence spectroscopy

Maintenance of energy balance under changeable light conditions is an essential function of photosynthetic organisms to achieve efficient photochemical reactions. Among the photosynthetic organisms, diatoms possess light-harvesting fucoxanthin chlorophyll (Chl) a/c-binding protein (FCP) as peripheral antennas. However, how diatoms regulate excitation-energy distribution between FCP and the two photosystem cores during light adaptation is poorly understood. In this study, we examined spectroscopic properties of a marine diatom Chaetoceros gracilis adapted in the dark and at photosynthetic photon flux density at 30 and 300 μmol photons m−2 s−1. Absorption spectra at 77 K showed significant changes in the Soret region, and 77-K steady-state fluorescence spectra showed significant differences in the spectral shape and relative fluorescence intensity originating from both PSII and PSI, among the cells grown under different light conditions. These results suggest alterations of pigment composition and their interactions under the different light conditions. These alterations affected the excitation-energy dynamics monitored by picosecond time-resolved fluorescence analyses at 77 K significantly. The contributions of Chls having lower energy levels than the reaction center Chls in the two photosystems to the energy dynamics were clearly identified in the three cells but with presumably different roles. These findings provide insights into the regulatory mechanism of excitation-energy balance in diatoms under various light conditions.

Synaptic Regulation of Metabolism.

Neurons in the brain, particularly those in the hypothalamus, are essential for the maintenance of whole-body metabolic homeostasis. Dysfunctions or dysregulations of them can result in various metabolic diseases, including eating disorders, obesity, and diabetes. In addition to hormonal and peptidergic regulation, accumulating evidence has shown that these neurons are subject to synaptic regulation, which has been largely overlooked. In this chapter, we focus on synaptic neurotransmission of hypothalamic neurons and summarize current knowledge of synaptic plasticity in the maintenance of energy balance. Synaptic modulation engaged by circulating hormones is also discussed.