Appetite Control Research Articles

AgRP Neuron-Specific Ablation Represses Appetite, Energy Intake, and Somatic Growth in Larval Zebrafish

Neuronal circuits regulating appetite are dominated by arcuate nucleus neurons, which include appetite-promoting and -suppressing neurons that release the orexigenic neuropeptide agouti-related protein (AgRP) and anorexigenic neuropeptide pro-opiomelanocortin, respectively, to compete for melanocortin receptors to modulate feeding behavior. In this study, we expressed novel agrp promoters, including different lengths of the 5' flanking regions of the agrp gene (4749 bp) in the zebrafish genome. We used the agrp promoter to derive the enhanced green fluorescent protein (EGFP)-nitroreductase (NTR) fusion protein, allowing expression of the green fluorescence signal in the AgRP neurons. Then, we treated the transgenic zebrafish AgRP4.7NTR (Tg [agrp-EGFP-NTR]) with metronidazole to ablate the AgRP neurons in the larvae stage and observed a decline in their appetite and growth. The expression of most orexigenic and growth hormone/insulin-like growth factor axis genes decreased, whereas that of several anorexigenic genes increased. Our findings demonstrate that AgRP is a critical regulator of neuronal signaling for zebrafish appetite and energy intake control. Thus, AgRP4.7NTR can be used as a drug-screening platform for therapeutic targets to treat human appetite disorders, including obesity. Furthermore, the unique agrp promoter we identified can be a powerful tool for research on AgRP neurons, especially AgRP neuron-mediated pathways in the hypothalamus, and appetite.

Whole Transcriptome Analysis of Hypothalamus in Mice during Short-Term Starvation

Molecular profiling of the hypothalamus in response to metabolic shifts is a critical cue to better understand the principle of the central control of whole-body energy metabolism. The transcriptional responses of the rodent hypothalamus to short-term calorie restriction have been documented. However, studies on the identification of hypothalamic secretory factors that potentially contribute to the control of appetite are lacking. In this study, we analyzed the differential expression of hypothalamic genes and compared the selected secretory factors from the fasted mice with those of fed control mice using bulk RNA-sequencing. We verified seven secretory genes that were significantly altered in the hypothalamus of fasted mice. In addition, we determined the response of secretory genes in cultured hypothalamic cells to treatment with ghrelin and leptin. The current study provides further insights into the neuronal response to food restriction at the molecular level and may be useful for understanding the hypothalamic control of appetite.

The complex pattern of the effects of prolonged frequent exercise on appetite control, and implications for obesity

From a public health perspective, much of the interest in the relationship between exercise and appetite rests on the implications for energy balance and obesity. Energy balance reflects a dynamic 2-way interaction between energy expenditure (EE) and energy intake (EI). Physical activity and exercise, and appetite are the behavioural components of EE and EI, respectively. Beyond EE, exercise is a powerful and complex physiological stimulus acting on several bodily systems. There are multiple effects of frequent and prolonged exercise on appetite which include inter alia an increase in fasting hunger, an enhancement of post-prandial satiety, a modulation of the hedonic responses to food and improvements in eating behaviour traits. These lead to variable adjustments in EI and in a reduction in the susceptibility to overconsumption. Frequent and prolonged physical activity and exercise behaviour can strengthen and sensitise the appetite control system, whilst physical inactivity and sedentariness (low level of EE) fails to downregulate EI and can permit overconsumption. Not all of the effects of exercise operate uniformly to drive appetite in the same direction. The complexity of the interaction between EE and EI means that the effects of prolonged exercise are characterised by substantial individual heterogeneity. This leads to variable effects on energy balance and body mass.

Tanycyte, the neuron whisperer

Reciprocal communication between neurons and glia is essential for normal brain functioning and adequate physiological functions, including energy balance. In vertebrates, the homeostatic process that adjusts food intake and energy expenditure in line with physiological requirements is tightly controlled by numerous neural cell types located within the hypothalamus and the brainstem and organized in complex networks. Within these neural networks, peculiar ependymoglial cells called tanycytes are nowadays recognized as multifunctional players in the physiological mechanisms of appetite control, partly by modulating orexigenic and anorexigenic neurons. Here, we review recent advances in tanycytes' impact on hypothalamic neuronal activity, emphasizing on arcuate neurons.

The Effects of Insulin on Spike Activity of the Suprachiasmatic Nucleus Neurones and Functional State of Afferent Inputs from the Arcuate Nucleus in Rats

In experiments on the sagittal hypothalamic slices of male Wistar rats, the effects of 15 nM insulin on the level of spike activity, parameters of spike information coding by the suprachiasmatic nucleus neurones, and functional state of afferent inputs to the neurones from the arcuate nucleus were studied. Application of insulin induced a decrease in the frequency of action potential generation and an increase in the entropy of interspike interval distribution in 33.3% of neurones recorded; in 12% of cells, the responses of opposite direction were found; in the remaining 54.7% neurones, spike activity did not change. The responses of the entropy of interspike interval distribution suggest the related changes in a degree of interspike interval irregularity induced by insulin. To characterise afferent inputs to the suprachiasmatic nucleus neurones from the arcuate nucleus, electrophysiological technique of the construction and analysis of the peristimulus time histogram (PSTH) was used. Statistically significant responses to the stimulation of the arcuate nucleus were recorded in 24 of 38 neurones of the suprachiasmatic nucleus. In 6 of the neurones, the responses were in the form of a short-latency (20 ms) excitation, in 1 neurone in the form of a long-latency excitation, in 6 neurones in the form of a short-latency inhibition; in 11 neurones complex two- or three-phase responses in the form of different compositions of excitation and inhibition were observed. Application of 15 nM insulin induced a qualitative transformation of the responses (disappearing of the initial responses or emergence of new responses) in 5 neurones initially responded to stimulation, and in 1 neurone initially not responded to stimulation of the arcuate nucleus. Statistically significant changes in the latency or duration of the responses in the presence of insulin were not found. The results of the study suggest the ability of insulin to influence the activity level and the spike code of a respectively numerous population of neurones in the suprachiasmatic nucleus circadian oscillator as well as modulate the functional state of afferent inputs to the circadian oscillator from hypothalamic arcuate nucleus playing an important role in the control of appetite and metabolism.

Short, frequent high-intensity physical activity breaks reduce appetite compared to a continuous moderate-intensity exercise bout.

A single exercise session can affect appetite-regulating hormones and suppress appetite. The effects of short, regular physical activity breaks across the day on appetite are unclear. This study investigated the effects of breaking up sitting with high-intensity physical activity vs a single bout of moderate-intensity exercise and prolonged sitting on appetite control. In this randomised crossover trial, 14 sedentary, inactive adults (7 women) completed 3, 8-h experimental conditions: (i) prolonged sitting (SIT); (ii) 30 min of moderate-intensity exercise followed by prolonged sitting (EX-SIT), and (iii) sitting with 2 min 32 s of high-intensity physical activity every hour (SIT-ACT). Physical activity energy expenditure was matched between EX-SIT and SIT-ACT. Subjective appetite was measured every 30 min with acylated ghrelin and total peptide-YY (PYY) measured hourly in response to two standardised test meals. An ad libitum buffet meal was provided at the end of each condition. Based on linear mixed model analysis, total area under the curve for satisfaction was 16% higher (P = 0.021) and overall appetite was 11% lower during SIT-ACT vs EX-SIT (P = 0.018), with no differences between SIT-ACT and SIT. Time series analysis indicated that SIT-ACT reduced subjective appetite during the majority of the post-lunch period compared with SIT and EX-SIT, with some of these effects reversed earlier in the afternoon (P < 0.05). Total PYY and acylated ghrelin did not differ between conditions. Relative energy intake was 760 kJ lower during SIT-ACT vs SIT (P = 0.024). High-intensity physical activity breaks may be effective in acutely suppressing appetite; yet, appetite-regulating hormones may not explain such responses.

The 'hunger games' - Structural studies of the MC4 receptor reveal mechanism for satiety.

Obesity is a global epidemic causing increased morbidity and impaired quality of life. The melanocortin receptor 4 (MC4R) is at the crux of appetite, energy homeostasis, and body-weight control in the central nervous system and is a prime target for anti-obesity drugs. MC4R is a member of the GPCR superfamily and signals primarily through the heterotrimeric G protein Gs. Through combination of structural, biochemical and cellular studies we determined the cryo-EM structure of the human MC4R-Gs signaling complex, and explored the cellular conduits for signal transduction in health and disease. The work reveals the mechanism of MC4R activation, highlighting a molecular switch that signals satiation. These results fill a major gap in understanding MC4R activation and guide the design of future weight management drugs.

Association between the Timing of Pre-Workout Macronutrient Intake and Rated Appetite among Resistance-Trained Adults in Jbeil, Lebanon.

Macronutrients play an important role in appetite regulation. In addition, adequate nutrient and energy intake, which may be altered by exercise-induced appetite fluctuations, is required to ensure important training outcomes. However, findings regarding appetite responses to macronutrient consumption before training and to different resistance training intensities remain inconclusive. This study investigated the association of three types of macronutrient intake before different intensities of resistance training with appetite. A purposive cross-sectional design was used to collect data from 280 resistance-trained individuals (mean age 26.4 ± 5.8 years) representing five gyms located in Jbeil, Lebanon, and who completed an online questionnaire. Data collected included socio-demographics, nutritional strategies followed by each respondent, training characteristics, and appetite rating before, during and after exercise using a validated visual analogue scale (VAS). A short-term suppression of appetite was reported during resistance-training, with no significant difference in exercise intensities (p > 0.05). In addition, low-fiber carbohydrate and protein food/beverage content consumed 30-60 min before training had an advantage in appetite suppression. In summary, these findings suggest that resistance training combined with pre-workout consumption of a whole meal was associated with appetite suppression, at least during the short period of exercise. From the perspective of appetite control and energy balance, the critical factor is the quantity and quality of macronutrient food sources, in addition to the timing surrounding training of nutrients ingested.

When should I eat: A circadian view on food intake and metabolic regulation.

The circadian clock is a hierarchical timing system regulating most physiological and behavioral functions with a period of approximately 24 h in humans and other mammalian species. The circadian clock drives daily eating rhythms that, in turn, reinforce the circadian clock network itself to anticipate and orchestrate metabolic responses to food intake. Eating is tightly interconnected with the circadian clock and recent evidence shows that the timing of meals is crucial for the control of appetite and metabolic regulation. Obesity results from combined long-term dysregulation in food intake (homeostatic and hedonic circuits), energy expenditure, and energy storage. Increasing evidence supports that the loss of synchrony of daily rhythms significantly impairs metabolic homeostasis and is associated with obesity. This review presents an overview of mechanisms regulating food intake (homeostatic/hedonic) and focuses on the crucial role of the circadian clock on the metabolic response to eating, thus providing a fundamental research axis to maintain a healthy eating behavior.

Association between physical activity, growth differentiation factor 15 and bodyweight in older adults: A longitudinal mediation analysis

Late-life aging is often associated with appetite reduction and weight loss. Physical activity (PA) may prevent these processes, but the molecular mechanisms involved remain elusive. The present study investigated the putative mediating aspect of growth differentiation factor 15 (GDF-15), a stress signalling protein involved in aging, exercise and appetite control, on the association between PA and late-life-associated weight loss. One thousand eighty-three healthy adults (63.8% women) aged 70years and over who participated in the Multidomain Alzheimer Preventive Trial were included. Bodyweight (kg) and PA levels (square root of metabolic equivalent of task-min/week) were assessed repeatedly from baseline to the 3-year visit, whereas plasma GDF-15 (pg/mL) was measured at the 1-year visit. Multiple linear regressions were performed to test the association between first-year mean PA level, 1-year visit GDF-15 concentration and subsequent bodyweight changes. Mediation analyses were used to investigate whether GDF-15 mediated the association between first-year mean PA levels and consecutive bodyweight changes. Multiple regression analyses demonstrated that higher first-year mean PA levels significantly predicted lower GDF-15 and bodyweight at 1year (B=-2.22; SE=0.79; P=0.005). In addition, higher 1-year visit GDF-15 levels were associated with faster subsequent bodyweight loss (Time×GDF-15 interaction B=-0.0004; SE=0.0001; P=0.003). Mediation analyses confirmed that GDF-15 mediated the association between first-year mean PA levels and subsequent bodyweight changes (mediated effect ab=0.0018; bootstrap SE=0.001; P<0.05) and revealed that mean PA had no direct effect on subsequent bodyweight changes (c' =0.006; SE=0.008; P>0.05). This study suggests that GDF-15 may be one of the molecules mediating the link between PA and late-life weight loss, but mechanistic studies are necessary to further support the present findings.

Association of BDNF gene missense polymorphism rs6265 (Val66Met) with three quantitative traits, namely, intelligence quotient, body mass index, and blood pressure: A genetic association analysis from North India.

Brain-derived neurotrophic factor (BDNF), a neurotransmitter modulator, plays a significant role in neuronal survival and growth and participates in neuronal plasticity, thus being essential for learning, memory, and the development of cognition. Additionally, it is crucial for appetite, weight, and metabolic control and plays a pivotal role in the cardiovascular system. The Val66Met polymorphism (rs6265) of the BDNF gene causes a decrease in BDNF secretion and plays a role in impairments in cognition, energy homeostasis, and cardiovascular events. The present study aimed to evaluate the association of polymorphism (rs6265) of the BDNF gene with three quantitative traits simultaneously, namely, intelligence quotient (IQ), body mass index (BMI), and blood pressure (BP). Psychometric, morphometric, and physiometric data of the total participants (N = 246) were collected. WASI-IIINDIA was used to measure cognitive ability. Genotyping was carried out using allele-specific PCR for the rs6265 polymorphism (C196T), and genotypes were determined. Statistical analyses were performed at p < 0.05 significance level using MS-Excel and SigmaPlot. The odds ratio models with a 95% confidence interval were used to test the associations. The used models are co-dominant, recessive, dominant, over-dominant, and additive. The allelic frequencies of alleles C and T were 72 and 28%, respectively. Under the dominant genetic model, a significant susceptible association of minor allele T was observed with a lower average verbal comprehensive index (OR = 2.216, p = 0.003, CI (95%) =1.33-3.69), a lower average performance reasoning index (OR = 2.634, p < 0.001, CI (95%) = 1.573-4.41), and a lower average full-scale IQ-4 (OR = 3.159, p < 0.001, CI (95%) = 1.873-5.328). Carriers of Met-alleles were found to have an increased body mass index (OR = 2.538, p < 0.001, CI (95%) = 1.507-4.275), decreased systolic blood pressure (OR = 2.051, p = 0.012, CI (95%) = 1.202-3.502), and decreased diastolic blood pressure (OR = 2.162, p = 0.006, CI (95%) = 1.278-3.657). Under the recessive genetic model, several folds decrease in IQ and BP and an increase in BMI with the presence of the T allele was also detected. This novel study may improve our understanding of genetic alterations to the traits and hence be helpful for clinicians and researchers to investigate the diagnostic and prognostic value of this neurotrophic factor.

Effect of transcranial direct current stimulation on homeostatic and hedonic appetite control and mood states in women presenting premenstrual syndrome across menstrual cycle phases

PurposeThis study investigated the acute effect of anodal transcranial direct current stimulation (a-tDCS) over the left dorsolateral prefrontal cortex (DLPFC) on appetite, energy intake, food preferences, and mood states in the luteal and follicular phases of the menstrual cycle in women presenting premenstrual syndrome. MethodsSixteen women (26.5 ± 5.2 years; 1.63 ± 0.1 m; 64.2 ± 12.8 kg; body mass index 24.0 ± 5.0 kg/m2; body fat 27.6 ± 7.5%) with the eumenorrheic menstrual cycle were submitted to a-tDCS and sham-tDCS conditions over their follicular and luteal phases. At pre - and post-tDCS, hunger and desire to eat something tasty, (analogic visual scale), the profile of mood states (POMS), and the psychological components of food preferences (Leeds Food Preference Questionnaire-BR) were assessed. Participants recorded their food intake for the rest of the day using a diary log. ResultsThere was a trend towards main effect of condition for decreased implicit wanting for low-fat savory food after a-tDCS but not sham-tDCS regardless of menstrual cycle phase (p = 0.062). There was no effect for self-reported hunger, desire to eat, energy and macronutrient intake, and on other components of food preferences (explicit liking and wanting for low- and high-fat savory and sweet foods, implicit wanting for low- and high-fat sweet and high-fat savory food); as well as for mood states. ConclusionsAlthough no significant effects of a-tDCS were found, the present investigation provides relevant perspectives for future studies.

The Effectiveness ofNigella sativaand Ginger as Appetite Suppressants: An Experimental Study on Healthy Wistar Rats.

Obesity is a global pandemic that is associated with high morbidity and mortality. Natural herbs are commonly used for weight reduction and appetite suppression.Therefore, we aim to investigate therole and mechanism of Nigella sativa (NS) and ginger on weight reduction and appetite regulation. This experimental study was performedat Imam Abdulrahman Bin Faisal University. Twenty-five femalerats were distributedinto 5 groups: NS(oral 1000mg/kg),Ginger(500 mg/kg), NS-ginger(both interventions), a positive control(intraperitoneal 50 μg/kg Liraglutide),and a negative control. Each intervention was given for9 weeks. Food intake and body weight were assessed weekly. Serum lipid profile and peptides involved in appetite control (cholecystokinin (CCK), glucagon-like peptide 1(GLP-1), gastric inhibitory polypeptide (GIP), ghrelin, peptide YY, and orexin) were assayed at the end of the experiment. None of the interventions showed a statistically significant difference regarding food consumption or weight gain (p > 0.05). However, the three interventions significantly reducedtotal cholesterol (TC), NS and NS-ginger significantly increased HDL, NS increased ghrelin and ginger increased orexin. The present dose and duration of NS, ginger, or in combination did not demonstrate a significant change inbody weight or food consumption in comparison to the negative or positive controls. However, NS or ginger has improved the lipid profile by reducing TC and increasing HDL. In addition, NS or ginger can influence some of the peptides involved in appetite regulation such as the increase in ghrelin induced by NS and the reduction of orexin induced by ginger. We believe that these latter effects are novel and might indicate a promising effect of these natural products on appetite regulation.

Are gastrointestinal signals the principal guides to human appetite and energy balance?

In view of the exponential rise of global obesity in the past three quarters of the century, it is useful to examine what is driving this change and what approaches can curb it. The chief drivers of weight gain are, on one hand our misunderstanding of the mechanisms controlling energy balance, and, on the other, reliance on current, potentially misleading conflicting scientific opinions and government policies regarding the controls of human appetite. This review outlines the evidence that: (1) there is no direct bioenergetic feedback from energy metabolism or energy stores to the brain mechanisms guiding feeding and energy expenditure, (2) human appetite is controlled by signals originating from an empty or full stomach, food palatability and opportunities to eat as well by the rate of food absorption, that (3) humans bear a genetic burden of having high ability and capacity to store fat and mechanisms that curb body- mass and fat loss, (4) humans are motivated to overconsume while maintaining low energy expenditure, and (5) commercial interests of food businesses marketing highly palatable foods, and wide-spread mechanization of living tasks and urban design reduce the need for physical work and movement. The non-pharmacological and non-surgical solutions to obesity involve an understanding of human genetic impediments and environmental obstacles to maintaining healthy weight, coupled with deliberate corrective or preventive behaviors, such as understanding and using gastrointestinal tract signals that provide sufficient, albeit subtle, cues for sensible food intake, and using daily weight monitoring and activity tracking devices to record and motivate healthy levels of physical activity.

Hypothalamic volume is associated with body mass index

The hypothalamus is an important neuroendocrine hub for the control of appetite and satiety. In animal studies it has been established that hypothalamic lesioning or stimulation causes alteration to feeding behaviour and consequently body mass, and exposure to high calorie diets induces hypothalamic inflammation. These findings suggest that alterations in hypothalamic structure and function are both a cause and a consequence of changes to food intake. However, there is limited in vivo human data relating the hypothalamus to obesity or eating disorders, in part due to technical problems relating to its small size. Here, we used a novel automated segmentation algorithm to exploratorily investigate the relationship between hypothalamic volume, normalised to intracranial volume, and body mass index (BMI). The analysis was applied across four independent datasets comprising of young adults (total n = 1,351 participants) spanning a range of BMIs (13.3 – 47.8 kg/m2). We compared underweight (including individuals with anorexia nervosa), healthy weight, overweight and obese individuals in a series of complementary analyses.We report that overall hypothalamic volume is significantly larger in overweight and obese groups of young adults. This was also observed for a number of hypothalamic sub-regions. In the largest dataset (the HCP-Young Adult dataset (n = 1111)) there was a significant relationship between hypothalamic volume and BMI.We suggest that our findings of a positive relationship between hypothalamic volume and BMI is potentially consistent with hypothalamic inflammation as seen in animal models in response to high fat diet, although more research is needed to establish a causal relationship. Overall, we present novel, in vivo findings that link elevated BMI to altered hypothalamic structure. This has important implications for study of the neural mechanisms of obesity in humans.

Cannabinoids: new friends in bone fracture and in joint disease prevention?

n recent years the endocannabinoid system (ES) has been recognized to play an important role in the regulation of several physiological processes, including pain perception, appetite control, and motor function development. This system has recently been recognized to be present in bone and joint tissues, playing a role in the regulation of bone and joint physiology. The ES seems to play its role mainly by acting on its receptors and thanks to the demonstrated ability of bone cells to synthesize the principal endocannabinoids (i.e., anandamide and 2-arachidonoylglycerol), which can act on bone remodeling and metabolism. Cannabinoids have also been shown to be produced within synovial tissues, and recent studies have shown that cannabinoid receptor ligands are effective in the treatment of inflammatory arthritis. In recent years synthetic endocannabinoid-like compounds and phytocannabinoids, which are the principal components of Cannabis sativa, have also started to be studied as molecules that could play a role not only in bone physiology, but also in the pathogenesis of osteoporosis, the most common bone disease, and in the inflammatory processes underlying osteoarthritis. Accumulating evidence that cannabinoids and their receptors play an important role in bone metabolism and in the regulation of the immune response is now starting to show us the true future therapeutic potential of cannabinoids, and of the phytocannabinoids contained in Cannabis sativa, in the treatment of bone loss and joint diseases. Here we summarize the role of the cannabinoids and their receptors in bone metabolism, osteoporosis, and joint disease.

Effects of acute exercise and exercise training on plasma GDF15 concentrations and associations with appetite and cardiometabolic health in individuals with overweight or obesity – A secondary analysis of a randomized controlled trial

Growth Differentiation Factor 15 (GDF15) is seemingly involved in appetite control. Acute exercise increases GDF15 concentrations in lean humans, but acute and long-term effects of exercise on GDF15 in individuals with overweight/obesity are unknown. We investigated the effects of acute exercise and exercise training on GDF15 concentrations in individuals with overweight/obesity and associations with appetite and cardiometabolic markers. 90 physically inactive adults (20–45 years) with overweight/obesity were randomized to 6-months habitual lifestyle (CON, n=16), or isocaloric exercise of moderate (MOD, n=37) or vigorous intensity (VIG, n=37), 5 days/week. Testing was performed at baseline, 3, and 6 months. Plasma GDF15 concentrations, other metabolic markers, and subjective appetite were assessed fasted and in response to acute exercise before an ad libitum meal. Cardiorespiratory fitness, body composition, insulin sensitivity, and intraabdominal adipose tissue were measured. At baseline, GDF15 increased 18% (95%CI: 4; 34) immediately after acute exercise and 32% (16; 50) 60 min post-exercise. Fasting GDF15 increased 21% (0; 46) in VIG after 3 months (p=0.045), but this attenuated at 6 months (13% (−11; 43), p=0.316) and was unchanged in MOD (11% (−6; 32), p=0.224, across 3 and 6 months). Post-exercise GDF15 did not change in MOD or VIG. GDF15 was not associated with appetite or energy intake. Higher GDF15 was associated with lower cardiorespiratory fitness, central obesity, dyslipidemia, and poorer glycemic control. In conclusion, GDF15 increased in response to acute exercise but was unaffected by exercise training. Higher GDF15 concentrations were associated with a less favorable cardiometabolic profile but not with markers of appetite. This suggests that GDF15 increases in response to acute exercise independent of training state. Whether this has an impact on free-living energy intake and body weight management needs investigation.

Acute impact of light at night and exogenous melatonin on subjective appetite and plasma leptin.

This study investigates the possible effect of exogenous melatonin on appetite control by investigating plasma leptin and subjective appetite parameters. Nine healthy male participants [26 ± 1.3 years, body mass index (BMI) 24.8 ± 0.8 kg/m2] (mean ± SD) were recruited. The study was designed as a randomized three-way cross-over design; light (>500 lux) (LS), dark (<5 lux) + exogenous melatonin (DSC), and light (>500 lux) + exogenous melatonin (LSC), with an interval of at least 7 days between each session. Each session started at 18:00 h and ended at 06:00 h the following day. Participants were awake and in a semi-recumbent position during each clinical session. The meal times were individualized according to melatonin onset from 48 h sequential urine collection, whereas melatonin intake was given 90 min before the evening meal. Subjective appetite parameters were collected at 30 min intervals during each session. Plasma leptin was collected at specific time points to analyze pre-prandial and postprandial leptin. Subjective hunger and desire to eat were reported higher in LS than DSC and LSC (P = 0.03, and P = 0.001). Plasma leptin showed a significant increase in LSC and DSC (p = 0.007). This study suggested a positive impact of exogenous melatonin on subjective appetite and plasma leptin.

Role of G-protein coupled receptor (GPCRs)/(GPR-120) as an agonists in diabetic wound healing

Type 2 diabetes (T2D) or Obesity has been gradually rising throughout the globe. It is a major cause of noncommunicable illnesses such as cardiovascular disease type 2 diabetes (T2D), Nonalcoholic Steatohepatitis (NASH), nonalcoholic fatty liver disease (NAFLD), and numerous malignancies, all of which have a negative effect on quality of natural life and life expectancy. Diabetic wound healing is hampered by a complicated pathophysiology combining immunological, metabolic factors and neuropathic. There are more than thirty GPCRs that have been occupied in the expansion or development of β-cell disfunction, insulin resistance, obesity, and T2DM Still, at current, only the GLP-1R has been effectively battered therapeutically. They play major function in gut hormone Secretion and appetite control adipogenesis, anti-inflammatory functions, antidiabetic functions. Diabeties is current treated by dressings, antidiabetic Drugs, growth factors such as (TGF1, FGF, EGF, VEGF and PDGF). Future therapeutic strategies will be based on single growth factor, multiple growth factor, skin, cytokine enhancer, cytokine antagonist, matrix metalloproteinase antagonist, gene therapy and stem cell therapy, extracellular matrix and angiogenesis. • GPCRs, transmit their signals mostly via the alpha subunits and Ga12/13, Gai/o, Gas, and Gaq/11, are the four main functional characteristics of their alpha subunits. • GPCRs, as indicated in the genesis or evolution of – insulin resistance, obesity and cell dysfunction, encouraged (T2DM). • GPCRs including as GPR65, GPR4, GPR132, and GPR68, are implicated in wound healing. • GPR120 is strongly stated in enteroendocrine cells, which promotes stomach inhibitory peptide production (GIP) and engaged in a well-coordinated anti-diabetic action.

Enteroendocrine Systems That Sense Nutrients in the Gut and Control the Body.

Gut hormones produced and released from enteroendocrine cells have key roles not only in nutrient digestion and absorption, but also in control of appetite, nutrient deposition and storage in the body. Several types of enteroendocrine cells sense nutrients after meal ingestion and release specific gut hormones. Understanding how gut hormone responses are controlled and in turn regulate physiological outcomes is an area of active research. In addition, the role of the endocrine system in human-physiology and in pathophysiology (obesity, diabetes, and gastrointestinal diseases) has begun being investigated. The symposium was organized to present and discuss recent advances in this research field from the aspects of bench to bedside.