Greater lactate accumulation does not alter peripheral concentrations of key appetite-regulating neuropeptides.

The potential mechanisms involved in lactate's role in exercise-induced appetite suppression requires further examination. We used sodium bicarbonate (NaHCO3) supplementation in a double-blind, placebo controlled, randomized crossover design to explore lactate's role on neuropeptide Y (NPY), agouti-related peptide (AgRP), and alpha-melanocyte stimulating hormone (α-MSH) concentrations. Twelve adults (7 males; 24.2±3.4 kg‧m-2; 42.18±8.56 mL‧kg-1‧min-1) completed two identical high-intensity interval training sessions following ingestion of NaHCO3 (BICARB) or sodium chloride (PLACEBO) pre-exercise. Blood lactate, acylated ghrelin, NPY, AgRP, α-MSH, and appetite perceptions were measured pre-exercise, 0-, 30-, 60-, and 90-min post-exercise. Free-living energy intake (electronic food diaries) was measured the day before, of, and after each experimental session. In BICARB, blood lactate was greater post-exercise (p<0.002, d>0.70) though acylated ghrelin was similar (p=0.075, =0.206) at all time-points post-exercise (p>0.034, d<0.22). NPY (p=0.006, >0.509) and AgRP (p<0.001, >0.488) had main effects of time increasing following exercise and returning to baseline, with no differences between sessions (NPY: p=0.0.192, =0.149; AgRP: p=0.422, =0.060). α-MSH had no main effect of time (p=0.573, =0.063) or session (p=0.269, =0.110). Appetite perceptions were similar during BICARB and PLACEBO (p=0.007, d=0.28) increasing in both sessions post-exercise (p<0.088, d>0.57). Energy intake had a main effect of day (p=0.025, =0.825), where the experimental session day was greater than the day before (p=0.010, d=0.59) with no other differences between days (p>0.260, d<0.38). The lower accumulation of lactate than our previous work did not generate exercise-induced appetite suppression as there were no differences in acylated ghrelin, appetite perceptions, or peripheral concentrations of neuropeptides.

The effects of acute aerobic exercise on appetite-regulating parameters and energy intake in males with obesity.

Objective: To investigate the effects of moderate-intensity aerobic exercise on appetite control parameters, appetite perceptions, and energy intake in sedentary males with obesity. Design: Eleven males with obesity (body fat percentage 36.5 ± 2.5%, body mass index 35.3 ± 4.2 kg/m2, V̇O2peak 29 ± 3.1 mL·kg-1·min-1) completed two experimental sessions: (1) no exercise (CTRL) and (2) 60 min of moderate-intensity cycling exercise at 60% V̇O2peak (MICT) in a crossover design. Blood analysis included growth differentiation factor 15 (GDF-15), total ghrelin, peptide tyrosine tyrosine3-36 (PYY3-36), total glucagon-like peptide-1 (GLP-1), insulin, and glucose, as well as subjective appetite perceptions were measured in specific intervals. A standard breakfast at 0 h and an ad libitum meal postexercise was provided. Result: GDF-15 (95% confidence interval [CI]: [2.48-27.28] ng/L, p = 0.021) increased immediately following MICT compared to CTRL. However, there were no differences for PYY3-36 (p = 0.480, η p 2 = 0.025 ), total ghrelin (p = 0.646, η p 2 = 0.011 ), and total GLP-1 (p = 0.451, η p 2 = 0.029 ) between sessions. Appetite perceptions (95% CI: [(-20.38)-(-6.16)] mm, p = 0.001) were suppressed following MICT though energy intake was not different between the sessions (95% CI: [(-1904.9)-928.1] kJ, p = 0.480). Conclusion: Sixty minutes of MICT increased GDF-15 while suppressing appetite perceptions in individuals with obesity. There was no energy compensation postexercise.

Rediscovering a Forgotten Link: TSPO and RIM-BP1 in Appetite Regulation.

The translocator protein of 18 kDa (TSPO) and RIM binding protein 1 (RIM-BP1) are both heavily expressed in neurons at the olfactory bulb. These proteins have overlapping functional profiles and are both implicated in the development of obesity. Over 20 years ago, a yeast 2-hybrid experiment discovered that RIM-BP1 interacts with a peptide constructed from a fraction of the TSPO sequence. Considering these data, the authors predict that the interaction between RIM-BP1 and TSPO could alter the olfactory system's mediation of appetite. Despite the therapeutic potential of this interaction, it has never been confirmed if the full TSPO protein and RIM-BP1 interact. The interaction is instead often cited as physiologically irrelevant. This commentary revisits the forgotten interaction between TSPO and RIM-BP1, reviewing all relevant literature discussing their relationship. Contrary to common discourse that the RIM-BP1 and TSPO are potential binding partners, while the interaction may regulate many neurological functions, existing evidence suggests that the interaction would have a specific role in odor-guided appetite. Further research into the nutritional neuroscientific consequences of TSPO/RIM-BP1 interactions should therefore be conducted.

Brain Perception of Different Oils on Appetite Regulation: An Anorectic Gene Expression Pattern in the Hypothalamus Dependent on the Vagus Nerve.

(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.

Microbiome and metabolome analyses indicate variations in the gut microbiota that disrupt regulation of appetite.

The mechanism connecting gut microbiota to appetite regulation is not yet fully understood. This study identifies specific microbial community and metabolites that may influence appetite regulation. In the initial phase of the study, mice were administered a broad-spectrum antibiotic cocktail (ABX) for 10 days. The treatment significantly reduced gut microbes and disrupted the metabolism of arginine and tryptophan. Consequently, ABX-treated mice demonstrated a notable reduction in feed consumption. The hypothalamic expression levels of CART and POMC, two key anorexigenic factors, were significantly increased, while orexigenic factors, such as NPY and AGRP, were decreased. Notably, the levels of appetite-suppressing hormone cholecystokinin in the blood were significantly elevated. In the second phase, control mice were maintained, while the ABX-treated mice received saline, probiotics, and short-chain fatty acids (SCFAs) for an additional 10 days to restore their gut microbiota. The microbiota reconstructed by probiotic and SCFA treatments were quite similar, while microbiota of the naturally recovering mice demonstrated greater resemblance to that of the control mice. Notably, the abundance of Akkermansia and Bacteroides genera significantly increased in the reconstructed microbiota. Moreover, microbiota reconstruction corrected the disrupted arginine and tryptophan metabolism and the abnormal peripheral hormone levels caused by ABX treatment. Among the groups, SCFA-treated mice had the highest feed intake and NPY expression. Our findings indicate that gut microbes, especially Akkermansia, regulate arginine and tryptophan metabolism, thereby influencing appetite through the microbe-gut-brain axis.

Exercise-induced appetite suppression: An update on potential mechanisms.

The first systematic reviews of the effects of exercise on appetite-regulation and energy intake demonstrated changes in appetite-regulating hormones consistent with appetite suppression and decreases in subsequent relative energy intake over a decade ago. More recently, an intensity-dependent effect and several potential mechanisms were proposed, and this review aims to highlight advances in this field. While exercise-induced appetite suppression clearly involves acylated ghrelin, glucagon-like peptide-1 may also be involved, though recent evidence suggests peptide tyrosine tyrosine may not be relevant. Changes in subjective appetite perceptions and energy intake continue to be equivocal, though these results are likely due to small sample sizes and methodological inconsistencies. Of the proposed mechanisms responsible for exercise-induced appetite suppression, lactate has garnered the most support through in vitro and in vivo rodent studies as well as a growing amount of work in humans. Other potential modulators of exercise-induced appetite suppression may include sex hormones, growth-differentiation factor 15, Lac-Phe, brain-derived neurotrophic factor, and asprosin. Research should focus on the mechanisms responsible for the changes and consider these other modulators (i.e., myokines/exerkines) of appetite to improve our understanding of the role of exercise on appetite regulation.

Preparation and Preclinical Characterization of a Simple Ester for Dual Exogenous Supply of Lactate and Beta-hydroxybutyrate.

Elevation of the plasma levels of (S)-lactate (Lac) and/or (R)-beta-hydroxybutyrate (BHB) occurs naturally in response to strenuous exercise and prolonged fasting, respectively, resulting in millimolar concentrations of these two metabolites. It is increasingly appreciated that Lac and BHB have wide-ranging beneficial physiological effects, suggesting that novel nutritional solutions, compatible with high-level and/or sustained consumption, which allow direct control of plasma levels of Lac and BHB, are of strong interest. In this study, we present a molecular hybrid between (S)-lactate and the BHB-precursor (R)-1,3-butanediol in the form of a simple ester referred to as LaKe. We show that LaKe can be readily prepared on the kilogram scale and undergoes rapid hydrolytic conversion under a variety of physiological conditions to release its two constituents. Oral ingestion of LaKe, in rats, resulted in dose-dependent elevation of plasma levels of Lac and BHB triggering expected physiological responses such as reduced lipolysis and elevation of the appetite-suppressing compound N-L-lactoyl-phenylalanine (Lac-Phe).

Low temperature inhibits food intake via TRPA1 channel activation in Nile tilapia (Oreochromis niloticus).

Low temperatures significantly influence feeding behavior in ectothermic vertebrates, but the underlying mechanisms remain elusive. This study investigated the role of transient receptor potential ankyrin 1 (TRPA1) channels in mediating the appetite-suppressing effects of low temperature in Nile tilapia. TRPA1 was found to be highly expressed in the hypothalamus and co-localized with neuropeptide Y (NPY) neurons. Exposure to low temperatures reduced feeding frequency and increased TRPA1 expression. In vitro experiments demonstrated that low temperature and TRPA1 agonists induced calcium influx, which was blocked by a TRPA1 inhibitor. TRPA1 expression exhibited post-prandial increases and was downregulated by fasting. TRPA1 activation dose-dependently inhibited food intake, while its inhibition restored feeding suppressed by low temperature. TRPA1 activation downregulated orexigenic factors and upregulated anorexigenic factors through Ca2+/calmodulin-dependent pathways. These findings suggest that TRPA1 plays a crucial role in sensing low temperatures and regulating feeding behavior in tilapia.

Examining the Potential Applicability of Orexigenic and Anorexigenic Peptides in Veterinary Medicine for the Management of Obesity in Companion Animals.

This review article comprehensively explores the role of orexigenic and anorexigenic peptides in the management of obesity in companion animals, with a focus on clinical applications. Obesity in domestic animals, particularly dogs and cats, is prevalent, with significant implications for their health and well-being. Factors contributing to obesity include overfeeding, poor-quality diet, lack of physical activity, and genetic predispositions. Despite the seriousness of this condition, it is often underestimated, with societal perceptions sometimes reinforcing unhealthy behaviors. Understanding the regulation of food intake and identifying factors affecting the function of food intake-related proteins are crucial in combating obesity. Dysregulations in these proteins, whether due to genetic mutations, enzymatic dysfunctions, or receptor abnormalities, can have profound health consequences. Molecular biology techniques play a pivotal role in elucidating these mechanisms, offering insights into potential therapeutic interventions. The review categorizes food intake-related proteins into anorexigenic peptides (inhibitors of food intake) and orexigenic peptides (enhancers of food intake). It thoroughly examines current research on regulating energy balance in companion animals, emphasizing the clinical application of various peptides, including ghrelin, phoenixin (PNX), asprosin, glucagon-like peptide 1 (GLP-1), leptin, and nesfatin-1, in veterinary obesity management. This comprehensive review aims to provide valuable insights into the complex interplay between peptides, energy balance regulation, and obesity in companion animals. It underscores the importance of targeted interventions and highlights the potential of peptide-based therapies in improving the health outcomes of obese pets.

Circulating profile of the appetite-regulating hormone ghrelin during moult-fast and chick provisioning in southern rockhopper penguins (Eudyptes chrysocome chrysocome).

A multitude of animal species undergo prolonged fasting events at regularly occurring life history stages. During such periods of food deprivation, individuals need to suppress their appetite. The satiety signalling gut hormone ghrelin has received much attention in this context in studies looking at mammalian systems. In wild birds, however, knowledge on the ghrelin system and its role during extended fasts is still scarce. In this study, we collected plasma samples for measurements of circulating ghrelin concentrations from adult southern rockhopper penguins (Eudyptes chrysocome chrysocome) during the three to four week-long moult-fast that they repeat annually to replace their feathers. We further sampled chicks before and after feeding bouts and non-moulting adults. Circulating ghrelin levels did not differ significantly between fed and unfed chicks but chicks had significantly lower plasma ghrelin levels compared to adults. Furthermore, penguins in late moult (i.e. individuals at the end of the prolonged fasting bout) had higher ghrelin levels compared to non-moulting adults. Our results show elevated levels of circulating ghrelin during moult and generally lower levels of ghrelin in chicks than in adults regardless of feeding state. Given the scarcity or absence of knowledge on the function of ghrelin in seabirds and in fasting birds in general, our results add greatly to our understanding of the avian ghrelin system.

A non-microcystin-producing Microcystis wesenbergii strain alters fish food intake by disturbing neuro-endocrine appetite regulation.

Cyanobacterial harmful algal blooms (cHABs) are pervasive sources of stress resulting in neurotoxicity in fish. A member of the widely distributed Microcystis genus of bloom-forming cyanobacteria, Microcystis wesenbergii can be found in many freshwater lakes, including Dianchi Lake (China), where it has become one of the dominant contributors to the lake's recurrent blooms. However, unlike its more well-known counterpart M. aeruginosa, the effects of dense non-microcystin-containing M. wesenbergii blooms are seldom studied. The disturbance of appetite regulation and feeding behaviour can have downstream effects on the growth of teleost fish, posing a significant challenge to aquaculture and conservation efforts. Here we examined the effects of M. wesenbergii blooms on the food intake of Acrossocheilus yunnanensis, a native cyprinid in southern China. This fish species has disappeared in Dianchi Lake, and its reintroduction might be negatively affected by the presence of this newly-dominant Microcystis species. We co-cultured juvenile A. yunnanensis with a non-microcystin-producing strain of M. wesenbergii at initial densities between 5 × 104 and 1 × 106 cells/mL and monitored fish feeding behaviour and changes in neurotransmitter and hormone protein levels. High-density M. wesenbergii cultures increased the feeding rate of co-cultured fish, elevating concentrations of appetite-stimulating signalling molecules (Agouti-related protein and γ-aminobutyric acid), while decreasing inhibitory ones (POMC). These changes coincided with histopathological alterations and reduced somatic indices in brain and intestinal tissues. Given this potential for detrimental effects and dysregulation of food intake, further studies are necessary to determine the impacts of chronic exposure of M. wesenbergii in wild fish.

Host genetics and nutrition.

Optimal nutrition is essential for health and physiological performance. Nutrition-related diseases such as obesity and diabetes are major causes of death and reduced quality of life in modern Western societies. Thanks to combining nutrigenetics and nutrigenomics, genomic nutrition allows the study of the interaction between nutrition, genetics and physiology. Currently, interrelated multi-genetic and multifactorial phenotypes are studied from a multiethnic and multi-omics approach, step by step identifying the important role of pathways, in addition to those directly related to metabolism. It allows the progressive identification of genetic profiles associated with specific susceptibilities to diet-related phenotypes, which may facilitate individualised dietary recommendations to improve health and quality of life.

No Effect of High Eating Frequency Compared with Low Eating Frequency on Appetite and Inflammation Biomarkers: Results from a Randomized Crossover Clinical Trial.

BACKGROUND: Eating frequency (EF) focuses on the total number of eating occasions per day and may influence metabolic health. OBJECTIVES: We sought to examine the effect of high compared with low EF on appetite regulation and inflammatory biomarkers among healthy adults. METHODS: Data are from a randomized, crossover trial (the Frequency of Eating and Satiety Hormones study). Participants (n = 50) completed 2 isocaloric 21-d study periods of low EF (3 eating occasions/d) and high EF (6 eating occasions/d) in random order with a 14-d washout period in between. Participants were free-living and consumed their own food, using study-directed, structured meal plans with identical foods and total energy in both study periods. On days 1 and 21 of each EF period, fasting blood was collected during in-person clinic visits to assess plasma concentrations of ghrelin, leptin, adiponectin, and high-sensitivity C-reactive protein (hs-CRP). Linear mixed models with EF, diet sequence, and period as fixed effects and participant as random effect were used to estimate the intervention effect. Interaction effects between EF and body fat percentage were examined. RESULTS: Among the 50 participants who completed the trial, 39 (78%) were women, 30 (60%) were Non-Hispanic White, and 40 (80%) had a body mass index of <25 kg/m2, and the mean age was 32.1 y. The differences between high and low EF in fasting ghrelin (geometric mean difference: 17.76 ng/mL; P = 0.60), leptin (geometric mean difference: 2.09 ng/mL; P = 0.14), adiponectin (geometric mean difference: 381.7 ng/mL; P = 0.32), and hs-CRP (geometric mean difference: -0.018 mg/dL; P = 0.08) were not statistically significant. No significant interaction was observed between EF and body fat percentage on appetite regulation and inflammatory biomarkers. CONCLUSIONS: No differences was observed in fasting ghrelin, leptin, adiponectin, and hs-CRP comparing high and low EF. Future studies are needed to understand the physiology of EF and appetite as they relate to metabolic health. This trial was registered at clinicaltrials.gov as NCT02392897.

Overview of growth differentiation factor 15 (GDF15) in metabolic diseases.

GDF15 is a stress response cytokine and a distant member of the transforming growth factor beta (TGFß) superfamily, its levels increase in response to cell stress and certain diseases in the serum. To exert its effects, GDF15 binds to glial-derived neurotrophic factor (GDNF) receptor alpha-like (GFRAL), which was firstly identified in 2017 and highly expressed in the brain stem. Many studies have demonstrated that elevated serum GDF15 is associated with anorexia and weight loss. Herein, we focus on the biology of GDF15, specifically how this circulating protein regulates appetite and metabolism in influencing energy homeostasis through its actions on hindbrain neurons to shed light on its impact on diseases such as obesity and anorexia/cachexia syndromes. It works as an endocrine factor and transmits metabolic signals leading to weight reduction effects by directly reducing appetite and indirectly affecting food intake through complex mechanisms, which could be a promising target for the treatment of energy-intake disorders.

Correlation of Leptin in Patients With Type 2 Diabetes Mellitus.

The exponential increase in diabetes mellitus (DM) poses serious public health concerns. In this review, we focus on the role of leptin in type 2 DM. The peripheral actions of leptin consist of upregulating proinflammatory cytokines which play an important role in the pathogenesis of type 2 DM and insulin resistance. Moreover, leptin is known to inhibit insulin secretion and plays a significant role in insulin resistance in obesity and type 2 DM. A literature search was conducted on Medline, Cochrane, Embase, and Google Scholar for relevant articles published until December 2023. The following search strings and Medical Subject Headings (MeSH terms) were used: "Diabetes Mellitus," "Leptin," "NPY," and "Biomarker." This article aims to discuss the physiology of leptin in type 2 DM, its glucoregulatory actions, its relationship with appetite, the impact that various lifestyle modifications can have on leptin levels, and, finally, explore leptin as a potential target for various treatment strategies.

Differential changes in appetite hormones post-prandially based on menstrual cycle phase and oral contraceptive use: A preliminary study.

This was a preliminary study that examined whether appetite regulation is altered during the menstrual cycle or with oral contraceptives. Ten naturally cycling females (NON-USERS) and nine tri-phasic oral contraceptive using females (USERS) completed experimental sessions during each menstrual phase (follicular phase: FP; ovulatory phase: OP; luteal phase: LP). Appetite perceptions and blood samples were obtained fasted, 30, 60, and 90 min post-prandial to measure acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and total peptide tyrosine tyrosine (PYY). Changes were considered important if p < 0.100 and the effect size was ≥medium. There appeared to be a three-way (group x phase x time) interaction for acylated ghrelin where concentrations appeared to be greater in USERS versus NON-USERS during the OP 90-min post-prandial and during the LP fasted, and 90-min post-prandial. In USERS, ghrelin appeared to be greater 90-min post-prandial in the OP versus the FP with no other apparent differences between phases. There were no apparent differences between phases in NON-USERS. There appeared to be a three-way interaction for PYY where concentrations appeared to be greater in USERS during the FP 60-min post-prandial and during the OP 30-min post-prandial. In USERS PYY appeared to be greater 60-min post-prandial during the OP versus the LP with no other apparent differences. There were no apparent differences between phases in NON-USERS. There appeared to be no effect of group or phase on GLP-1, or appetite perceptions. These data demonstrate small effects of menstrual cycle phase and oral contraceptive use on the acylated ghrelin and total PYY response to a standardized meal, with no effects on active GLP-1 or perceived appetite, though more work with a large sample size is necessary.

Betaine improves appetite regulation and glucose-lipid metabolism in mandarin fish (Siniperca chuatsi) fed a high-carbohydrate-diet by regulating the AMPK/mTOR signaling.

Diets with high carbohydrate (HC) was reported to have influence on appetite and intermediary metabolism in fish. To illustrate whether betaine could improve appetite and glucose-lipid metabolism in aquatic animals, mandarin fish (Siniperca chuatsi) were fed with the HC diets with or without betaine for 8 weeks. The results suggested that betaine enhanced feed intake by regulating the hypothalamic appetite genes. The HC diet-induced downregulation of AMPK and appetite genes was also positively correlated with the decreased autophagy genes, suggesting a possible mechanism that AMPK/mTOR signaling might regulate appetite through autophagy. The HC diet remarkably elevated transcriptional levels of genes related to lipogenesis, while betaine alleviated the HC-induced hepatic lipid deposition. Additionally, betaine supplementation tended to store the energy storage as hepatic glycogen. Our findings proposed the possible mechanism for appetite regulation through autophagy via AMPK/mTOR, and demonstrated the feasibility of betaine as an aquafeed additive to regulate appetite and intermediary metabolism in fish.

Influence of the gut microbiome on appetite-regulating neuropeptides in the hypothalamus: Insight from conventional, antibiotic-treated, and germ-free mouse models of anorexia nervosa.

Recent research highlights the profound impact of the gut microbiome on neuropsychiatric disorders, shedding light on its potential role in shaping human behavior. In this study, we investigate the role of the gut microbiome in appetite regulation using activity-based anorexia (ABA) mouse model of anorexia nervosa (AN) - a severe eating disorder with significant health consequences. ABA was induced in conventional, antibiotic-treated, and germ-free mice. Our results show the clear influence of the gut microbiome on the expression of four orexigenic (neuropeptide Y, agouti-related peptide, melanin-concentrating hormone, and orexin) and four anorexigenic peptides (cocaine- and amphetamine-regulated transcript, corticotropin-releasing hormone, thyrotropin-releasing hormone, and pro-opiomelanocortin) in the hypothalamus. Additionally, we assessed alterations in gut barrier permeability. While variations were noted in germ-free mice based on feeding and activity, they were not directly attributable to the gut microbiome. This research emphasizes that the gut microbiome is a pivotal factor in AN's appetite regulation beyond just dietary habits or physical activity.

The olfactory bulb: A neuroendocrine spotlight on feeding and metabolism.

Olfaction is the most ancient sense and is needed for food-seeking, danger protection, mating and survival. It is often the first sensory modality to perceive changes in the external environment, before sight, taste or sound. Odour molecules activate olfactory sensory neurons that reside on the olfactory epithelium in the nasal cavity, which transmits this odour-specific information to the olfactory bulb (OB), where it is relayed to higher brain regions involved in olfactory perception and behaviour. Besides odour processing, recent studies suggest that the OB extends its function into the regulation of food intake and energy balance. Furthermore, numerous hormone receptors associated with appetite and metabolism are expressed within the OB, suggesting a neuroendocrine role outside the hypothalamus. Olfactory cues are important to promote food preparatory behaviours and consumption, such as enhancing appetite and salivation. In addition, altered metabolism or energy state (fasting, satiety and overnutrition) can change olfactory processing and perception. Similarly, various animal models and human pathologies indicate a strong link between olfactory impairment and metabolic dysfunction. Therefore, understanding the nature of this reciprocal relationship is critical to understand how olfactory or metabolic disorders arise. This present review elaborates on the connection between olfaction, feeding behaviour and metabolism and will shed light on the neuroendocrine role of the OB as an interface between the external and internal environments. Elucidating the specific mechanisms by which olfactory signals are integrated and translated into metabolic responses holds promise for the development of targeted therapeutic strategies and interventions aimed at modulating appetite and promoting metabolic health.

Differences in the levels of the appetite peptides ghrelin, peptide tyrosine tyrosine, and glucagon-like peptide-1 between obesity classes and lean controls.

OBJECTIVE: This study was designed to compare basal concentrations of the gastrointestinal appetite modulators ghrelin, peptide tyrosine tyrosine (PYY), and glucagon-like peptide 1 (GLP-1) between obesity classes and obesity classes and controls. METHODS: The study included 49 healthy controls with body mass index (BMI) between 18.5 and 29.9 kg/m² and 62 individuals with obesity with BMI ≥30 kg/m². Basal ghrelin, PYY, and GLP-1 concentrations of the samples were analyzed by an enzyme-linked immunosorbent assay commercial kit (SunRed Human). Other biochemical parameters were measured by a clinical chemistry autoanalyzer (Beckman Coulter AU 5800) in the biochemistry laboratory. RESULTS: Compared with the control group, ghrelin, PYY, and GLP-1 levels were significantly lower in the obese group (P < .05). The PYY concentration was significantly different between obese groups (P < .05). The PYY and GLP-1 levels were significantly different between obesity class I and obesity class III. In addition, ghrelin levels were significantly different between obesity class II and obesity class III. Correlation analysis revealed a negative correlation between BMI and serum ghrelin, GLP-1, and PYY concentrations. CONCLUSION: Low basal ghrelin, GLP-1, and PYY hormones in the obese group compared with the control group indicate impaired appetite regulation in this population. The significant difference in PYY levels between obese groups was associated with increasing obesity grade.