Modulation Of Appetite Research Articles

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 invitro and invivo 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.

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

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. 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. 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. 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.

Recent advances in the extraction, purification, structural-property correlations, and antiobesity mechanism of traditional Chinese medicine-derived polysaccharides: a review.

Traditional Chinese medicine (TCM) has displayed preventive and therapeutic effects on many complex diseases. As natural biological macromolecules, TCM-derived antiobesogenic polysaccharides (TCMPOs) exhibit notable weight-loss effects and are seen to be a viable tactic in the fight against obesity. Current studies demonstrate that the antiobesity activity of TCMPOs is closely related to their structural characteristics, which could be affected by the extraction and purification methods. Therefore, the extraction, purification and structural-property correlations of TCMPOs were discussed. Investigation of the antiobesity mechanism of TCMPOs is also essential for their improved application. Herein, the possible antiobesity mechanisms of TCMPOs are systematically summarized: (1) modulation of appetite and satiety effects, (2) suppression of fat absorption and synthesis, (3) alteration of the gut microbiota and their metabolites, and (4) protection of intestinal barriers. This collated information could provide some insights and offer a new therapeutic approach for the management and prevention of obesity.

FRI006 Appetite And Food Intake-regulating Hormones In Patients With Craniopharyngioma

Abstract Disclosure: C.S. Martins: None. M.C. Nogueira: None. A. Bueno: None. A.S. Berbel-Júnior: None. A.C. Moreira: None. S.R. Antonini: None. M. De Castro: None. Purpose: In patients with adamantinomatous craniopharyngiomas (aCP), hypothalamic obesity may occur due to hypothalamic involvement by the tumor or therapeutic interventions. Studies on appetite sensations and modulation of orexigenic and anorexigenic hormones may contribute to understand the pathogenesis of obesity in aCP patients. Patients and Methods: Fifteen patients (9F, 6M; 31.1±12.0 years) presenting aCP submitted to surgical resection and 15 controls paired by sex, age (31±11.7 years) and Body Mass Index (BMI) were evaluated. Leptin and adiponectin were measured in basal conditions, whereas glucose, insulin, GLP-1, PYY and ghrelin levels were assessed in basal conditions and 30, 60, 120 and 180 minutes after a standard meal test consisted by 70 g of hyposodic soy protein isolate-based powder diluted in 250 mL water to be consumed in up to 10 minutes, resulting in a drink of 315 Kcal with 44.1 g carbohydrate, 10.5 g fat, and 11.0 g protein (56%, 30%, and 14% of total calories, respectively). At the same time points, sensations of hunger, fullness and prospective food consumption were measured by a Visual Analogic Scale (VAS) composed of horizontal lines. Individuals were asked to mark across the line the point correspondent to their sensations, and the distance to the left end of the line was quantified. The term “hunger” was evaluated by the question “How much hunger do you feel?” The answers at the VAS were “I’m not hungry at all” and “I’ve never been so hungry.” The feeling of fullness was evaluated by the question “How satisfied are you?” and the answers were “I am completely empty” and “I am completely full.” Prospective consumption was evaluated by the question “How much do you think you can eat?” and the answers were “nothing” and “too much”. Results: Patients’ BMI were 30.9 ± 7.6 kg/m2. In aCP patients, differently from controls, the decrease of hunger from baseline to 60 minutes after the meal was not observed, demonstrating a more transient reduction in the sensation of hunger. In addition, a decrease of fullness sensation from 30 to 120 minutes (p=0.03) was observed, demonstrating a less durable sensation of fullness. There was a tendency towards higher fasting leptin concentrations in patients with aCP (p=0.06), while adiponectin levels were lower in patients (p=0.002). Insulin (p=0.01) and HOMA-IR (p=0.001) were higher in aCP patients compared to controls at 3 hours after meal, whereas GLP-1 (P=0.03) and PYY (p=0.02) were higher at 2 hours after the meal. PYY and ghrelin showed earlier postprandial rise and fall, respectively, in aCP patients. Conclusions: After the test, aCP patients exhibited more transient reduction in the sensation of hunger and less durable sensation of fullness than controls. Changes in appetite sensations and unregulated secretion of orexigenic and anorexigenic hormones may contribute to increased food intake and to the pathogenesis of obesity in aCP patients. Presentation: Friday, June 16, 2023

PACAP and VIP Neuropeptides' and Receptors' Effects on Appetite, Satiety and Metabolism.

The overwhelming increase in the prevalence of obesity and related disorders in recent years is one of the greatest threats to the global healthcare system since it generates immense healthcare costs. As the prevalence of obesity approaches epidemic proportions, the importance of elucidating the mechanisms regulating appetite, satiety, body metabolism, energy balance and adiposity has garnered significant attention. Currently, gastrointestinal (GI) bariatric surgery remains the only approach capable of achieving successful weight loss. Appetite, satiety, feeding behavior, energy intake and expenditure are regulated by central and peripheral neurohormonal mechanisms that have not been fully elucidated yet. Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) and Vasoactive Intestinal Polypeptide (VIP) are members of a family of regulatory peptides that are widely distributed in parallel with their specific receptors, VPAC1R, VPAC2R and PAC1R, in the central nervous system (CNS) and in the periphery, such as in the gastrointestinal tract and its associated organs and immune cells. PACAP and VIP have been reported to play an important role in the regulation of body phenotype, metabolism and homeostatic functions. The purpose of this review is to present recent data on the effects of PACAP, VIP, VPAC1R, VPAC2R and PAC1R on the modulation of appetite, satiety, metabolism, calorie intake and fat accumulation, to evaluate their potential use as therapeutic targets for the treatment of obesity and metabolic syndrome.

Pharmacological strategies for appetite modulation in eating disorders: a narrative review.

A substantial increase in the prevalence of eating disorders has been noticed over the past decades. Priority in the treatment of eating disorders is justifiably given to psychosocial interventions. However, it is also well known that centrally acting drugs can significantly affect appetite and food consumption. To narratively review the available neurobiological data on the mechanisms of central regulation of eating behavior as a rationale to summarize pharmacological strategies for appetite modulation in eating disorders. The authors have carried out a narrative review of scientific papers published from January 2013 to March 2023 in the PubMed and Web of Science electronic databases. Studies were considered eligible if they included data on the neurobiological mechanisms of appetite regulation or the results of clinical trials of centrally acting drugs in eating disorders. Relevant studies were included regardless of their design. Descriptive analysis was used to summarize the obtained data. The review included 51 studies. The available neurobiological and clinical data allowed us to identify the following pharmacological strategies for appetite modulation in eating disorders: serotonergic, catecholaminergic, amino acidergic and peptidergic. However, implementation of these data into clinical practice difficult due to an insufficient number of good-quality studies, which is particularly relevant for adolescents as there is a research gap in this population. The progress in neurobiological understanding of the mechanisms of central regulation of appetite opens opportunities for new pharmacotherapeutic approaches aimed at changing the patterns of eating behavior. Obviously, treatment of eating disorders is a much broader problem and cannot be reduced to the correction of eating patterns. Nevertheless, at certain stages of treatment, drug-induced modulation of appetite can play an important role among multi-targeted biological and psychosocial interventions. Translation of neurobiological data into clinical practice requires a large number of clinical studies to confirm the long-term efficacy and safety of pharmacotherapeutic approaches and to develop personalized algorithms for the treatment of various forms of eating disorders in different age groups.

Chronic spontaneous urticaria and metabolic syndrome: a relationship conundrum.

Chronic spontaneous urticaria (CSU) and metabolic syndrome (MetS) are associated with low-grade inflammation. Despite intensive research and various hypothesis, there is lack of specific pathomechanisms of urticaria. Previous studies have suggested low-grade inflammation in obesity which may be linked to urticaria. However, there is limited literature on association of MetS and CSU. So, this study was conducted to evaluate the association of MetS and its components in patients with CSU. This was a hospital-based and cross-sectional cohort study in which 481 patients of CSU and 240 age- and gender-matched controls were recruited. MetS was defined using the revised National Cholesterol Education Program Adult Treatment Panel III. BMI, waist circumference, blood pressure, fasting blood sugar, plasma insulin, and lipid profile were measured after overnight fasting. Pearson's Chi-squared test was used to calculate significance. Logistic regression analysis was done to assess MetS as a predictor of CSU. All patients were started on antihistamines according to the severity of the disease. CSU patients comprised 220 men (45.7%) and 261 women (54.3%) with 97 patients (20.12%) qualifying criteria for metabolic syndrome compared with 73 (30.42%) controls without any significant difference (p = 0.177). CSU was significantly associated with a higher prevalence of central obesity (p = 0.003) but CSU patients with central obesity did not have a higher urticaria activity score (p = 0.727) or serum IgE levels (p = 0.359). In conclusion, our study found an increased association of central obesity with CSU that was not related to the severity of urticaria. This is of significance as obesity is the most prevalent and first component of MetS to be developed. There was no increase in the overall prevalence of MetS in patients with CSU. The increased association of obesity and urticaria in our study can be partially explained by the role of antihistamines in modulation of metabolic pathway and appetite. Future research into the same can give better insights and thus can aid in better management options in CSU patients.

Internal and external modulation factors of the orexin system (REVIEW)

Orexin-A and -B (identical to hypocretin-1 and -2) are neuropeptides synthesized in the lateral hypothalamus and perifornical area, and orexin neurons project their axon terminals broadly throughout the entire central nervous system (CNS). The activity of orexins is mediated by two specific G protein-coupled receptors (GPCRs), termed orexin type1 receptor (OX1R) and orexin type2 receptor (OX2R). The orexin system plays a relevant role in various physiological functions, including arousal, feeding, reward, and thermogenesis, and is key to human health. Orexin neurons receive various signals related to environmental, physiological, and emotional stimuli. Previous studies have reported that several neurotransmitters and neuromodulators influence the activation or inhibition of orexin neuron activity. In this review, we summarize the modulating factors of orexin neurons in the sleep/wake rhythm and feeding behavior, particularly in the context of the modulation of appetite, body fluids, and circadian signaling. We also describe the effects of life activity, behavior, and diet on the orexin system. Some studies have observed phenomena that have been verified in animal experiments, revealing the detailed mechanism and neural pathway, while their applications to humans is expected in future research.

Butyrate in Human Milk: Associations with Milk Microbiota, Milk Intake Volume, and Infant Growth.

Butyrate in human milk (HM) has been suggested to reduce excessive weight and adipo-sity gains during infancy. However, HM butyrate's origins, determinants, and its influencing mechanism on weight gain are not completely understood. These were studied in the prospective longitudinal Cambridge Baby Growth and Breastfeeding Study (CBGS-BF), in which infants (n = 59) were exclusively breastfed for at least 6 weeks. Infant growth (birth, 2 weeks, 6 weeks, 3 months, 6 months, and 12 months) and HM butyrate concentrations (2 weeks, 6 weeks, 3 months, and 6 months) were measured. At age 6 weeks, HM intake volume was measured by deuterium-labelled water technique and HM microbiota by 16S sequencing. Cross-sectionally at 6 weeks, HM butyrate was associated with HM microbiota composition (p = 0.036) although no association with the abundance of typical butyrate producers was detected. In longitudinal analyses across all time points, HM butyrate concentrations were overall negatively associated with infant weight and adiposity, and associations were stronger at younger infant ages. HM butyrate concentration was also inversely correlated with HM intake volume, supporting a possible mechanism whereby butyrate might reduce infant growth via appetite regulation and modulation of HM intake.

The Role of Adipokines in Inflammatory Mechanisms of Obesity

Adipokines are currently widely studied cellular signaling proteins produced by adipose tissue and involved in various processes, including inflammation; energy and appetite modulation; lipid and glucose metabolism; insulin sensitivity; endothelial cell functioning; angiogenesis; the regulation of blood pressure; and hemostasis. The current review attempted to highlight the key functions of adipokines in the inflammatory mechanisms of obesity, its complications, and its associated diseases. An extensive search for materials on the role of adipokines in the pathogenesis of obesity was conducted online using the PubMed and Scopus databases until October 2022.

Phoenixin-14 alters transcriptome and steroid profiles in female green-spotted puffer (Dichotomyctere nigroviridis).

Phoenixin (PNX) is a highly conserved, novel hormone with diverse functions, including hypothalamic control of reproduction, appetite modulation, and regulation of energy metabolism and inflammation. While some functions appear conserved across vertebrates, additional research is required to fully characterize these complex pleiotropic effects. For instance, very little is known about transcriptome level changes associated with PNX exposure, including responses in the hypothalamic–pituitary–gonadal (HPG) axis, which is critical in vertebrate reproduction. In addition, the PNX system may be especially complex in fish, where an additional receptor is likely present in some species. The purpose of this study was to assess hypothalamic and ovarian transcriptomes after PNX-14 administration in female vitellogenic green-spotted puffer (Dichotomyctere nigroviridis). Steroid-related changes were also assessed in the liver and blood plasma. Hypothalamic responses included pro-inflammatory signals such as interleukin 1β, possibly related to gut–brain axis functions, as well as suppression of cell proliferation. Ovarian responses were more widely downregulated across all identified pathways, which may reflect progression to a less transcriptionally active state in oocytes. Both organs shared regulation in transforming growth factor-β and extracellular matrix remodeling (periostin) pathways. Reproductive processes were in general downregulated, but both inhibiting (bone morphogenetic protein 15 and follistatin) and promoting (17-hydroxyprogesterone) factors for oocyte maturation were identified. Select genes involved in reproduction (vitellogenins, estrogen receptors) in the liver were unresponsive to PNX-14 and higher doses may be needed to induce reproductive effects in D. nigroviridis. These results reinforce the complexity of PNX actions in diverse tissues and highlight important roles for this hormone in regulating the immune response, energy metabolism, and cell growth.

Apple Polyphenols Extracts Ameliorate High Carbohydrate Diet-Induced Body Weight Gain by Regulating the Gut Microbiota and Appetite.

To investigate the potential contribution of appetite regulation and modulation of gut microbiota to the ameliorated effects of apple polyphenols extracts (APE) on high carbohydrate diet (HCD)-induced body weight (BW) gain, we conducted this study. One hundred C57BL/6 male mice were randomly divided into seven groups and fed with the following diets for 12 weeks: chow diet (CON), HCD (HCD), high fructose and sucrose diet (HSCD), and HCD and HSCD with 125 or 500 mg/kg·day APE gavage. Compared to the CON group, the BW of mice in the HCD and HSCD groups increased significantly. HSCD induced a more significant weight gain in the white adipose tissue (WAT) and liver than HCD, accompanied by severe impairment of glucose tolerance and a larger diameter of adipocytes. On the other hand, by decreasing food intake, APE significantly reduced BW via mechanisms, including decreased weights of the WAT and liver, amelioration of glucose tolerance, and amplification of WAT browning by upregulating the mRNA levels of Ucp-1 and Cidea. Moreover, APE promoted transcription and secretion of GLP-1, with the increased expression of gut anorexigenic hormone peptides Ffar 2/3 in the colon and anorectic neuropeptide gene expression of Pomc, Cart, and Mc4r in the hypothalamus, causing increased satiety. Additionally, APE significantly increased Verrucomicrobia colonization and the relative abundance of Akkermansia. APE potentially ameliorates high simple carbohydrate diet-induced body weight gain by mechanisms related to gut microbiota regulation and appetite inhibition.

A Single Dose of Ginkgo biloba Extract Induces Gene Expression of Hypothalamic Anorexigenic Effectors in Male Rats

Previous studies have shown that Ginkgo biloba extract (GbE) reduces food intake and body mass gain and regulates proteins related to lipid metabolism in obese rats. In ovariectomized rats, GbE restored the hippocampal and hypothalamic serotonergic system activity, favoring the spontaneous feeding decrement. Considering the promising hypophagic effect of GbE, this study aimed to investigate the effect of a single acute dose on hypothalamic pathways that regulate feeding behavior in male rats. Four-month-old Wistar male rats received either a single acute oral GbE dose (500 mg/kg) or vehicle. Food intake and body mass were measured after 1, 4, 12, and 24 h. Rats were euthanized, and hypothalami were removed for mRNA quantification of anorexigenic (POMC/CART) and orexigenic (AgRP/NPY) neuropeptides, leptin/serotonin receptors (5HT1A, 5HT1B, 5HT2C), and serotonin transporters. We also investigated POMC, 5-HT1B, and 5-HT2C protein levels. A single acute GbE dose induced the hypothalamic POMC, CART, and 5-HT2C gene expression but failed to modify orexigenic effectors. No alterations in food intake, body mass, and hypothalamic protein levels were observed. In summary, the present findings demonstrate the rapid stimulation of pivotal hypothalamic anorexigenic pathways in response to a single GbE administration, reinforcing the GbE hypophagic activity. However, more studies are necessary to evaluate its potential as an appetite modulator.

Neurotrophin Receptor Kinase: Updated Perspectives, Laboratory Considerations, and Clinical Implications

Neurotrophin Receptor Kinase: Updated Perspectives, Laboratory Considerations, and Clinical Implications

Viral Infection Drives the Regulation of Feeding Behavior Related Genes in Salmo salar.

The feeding behavior in fish is a complex activity that relies on the ability of the brain to integrate multiple signals to produce appropriate responses in terms of food intake, energy expenditure, and metabolic activity. Upon stress cues including viral infection or mediators such as the proinflammatory cytokines, prostaglandins, and cortisol, both Pomc and Npy/Agrp neurons from the hypothalamus are stimulated, thus triggering a response that controls both energy storage and expenditure. However, how appetite modulators or neuro-immune cues link pathogenesis and energy homeostasis in fish remains poorly understood. Here, we provide the first evidence of a molecular linkage between inflammation and food intake in Salmon salar. We show that in vivo viral challenge with infectious pancreatic necrosis virus (IPNV) impacts food consumption by activating anorexic genes such as mc4r, crf, and pomcb and 5-HT in the brain of S. salar. At the molecular level, viral infection induces an overall reduction in lipid content in the liver, favoring the production of AA and EPA associated with the increment of elovl2 gene. In addition, infection upregulates leptin signaling and inhibits insulin signaling. These changes are accompanied by a robust inflammatory response represented by the increment of Il-1b, Il-6, Tnfa, and Pge2 as well as an increased cortisol level in vivo. Thus, we propose a model in which hypothalamic neurons respond to inflammatory cytokines and stress-related molecules and interact with appetite induction/inhibition. These findings provide evidence of crosstalk between pathogenesis-driven inflammation and hypothalamic–pituitary–adrenocortical axes in stress-induced food intake behavior in fish.

A Tale of Three Systems: Toward a Neuroimmunoendocrine Model of Obesity.

The prevalence of obesity is on the rise. What was once considered a simple disease of energy imbalance is now recognized as a complex condition perpetuated by neuro- and immunopathologies. In this review, we summarize the current knowledge of the neuroimmunoendocrine mechanisms underlying obesity. We examine the pleiotropic effects of leptin action in addition to its established role in the modulation of appetite, and we discuss the neural circuitry mediating leptin action and how this is altered with obesity, both centrally (leptin resistance) and in adipose tissues (sympathetic neuropathy). Finally, we dissect the numerous causal and consequential roles of adipose tissue macrophages in obesity and highlight recent key studies demonstrating their direct role in organismal energy homeostasis.

Associations of physical activity and sedentary behavior with appetite sensations and eating regulation behaviors before and during the initial year following bariatric surgery.

BackgroundBariatric surgery produces weight loss in part by impacting appetite and eating behavior. Research suggests physical activity (PA) assists with regulation of appetite and eating during non‐surgical weight loss, although whether PA carries similar benefits in the context of bariatric surgery is unknown.ObjectiveEvaluate associations of moderate‐to‐vigorous intensity PA (MVPA) and sedentary time (ST) with appetite sensations (hunger [homeostatic/hedonic], satiety) and eating regulation behaviors (restraint, disinhibition) before and during the initial year following bariatric surgery.MethodAdult bariatric patients received an accelerometer to measure MVPA/ST and a smartphone to complete appetite/eating ratings at four semi‐random times daily for 10 days at pre‐ and 3‐, 6‐, and 12‐months post‐surgery. Data were analyzed using generalized linear mixed models.ResultsHigher MVPA levels related to more satiety across time (p = 0.045) and more restraint at 3‐months post‐surgery (p < 0.001). At pre‐surgery, higher MVPA levels also related to more disinhibition (p's < 0.01), although participants reported more disinhibition on days they performed less MVPA than usual (p = 0.017). MVPA did not relate to hunger. Lower ST levels related to more hedonic hunger (p = 0.003), especially at 12‐months post‐surgery (p < 0.001), and participants reported more homeostatic hunger on days they accumulated more ST than usual (p = 0.044). Additionally, higher ST levels related to more disinhibition at 3‐months post‐surgery (p's < 0.01) and lower restraint at pre‐surgery (p's < 0.05). ST did not relate to satiety.ConclusionsThis study is the first to show that MVPA and ST each associate with appetite and eating regulation in daily life before and during post‐surgical weight loss. Results, while preliminary and requiring experimental confirmation, highlight potential for targeting bariatric patients' activity behaviors to enhance modulation of appetite, control of food intake, and resistance to overeating.

Metabolic Aspects of Five Commonly Used Non-Insulin Anti-Hyperglycemic Medications in Type 2 Diabetes

Type 2 diabetes is a growing public health challenge while carrying a significant health burden for the patient suffering from it. The worldwide prevalence of diabetes in 2019 was estimated to be 9.3%. Fortunately, a number of drug classes are now available for the medical management of hyperglycemia in this disorder. Metformin and the sulfonylureas are time-tested medications that are effective and inexpensive as first-line medications. The incretin-based therapies, namely the glucagon-like peptide-1 agents and the dipeptyl peptidase-4 inhibitors, offer novel mechanisms of gut hormone and appetite modulation. The former combine weight loss and cardiovascular benefit with glycemic control. The sodium glucose cotransporter-2 inhibitors have a unique glycosuric action that lowers glucose while being of value in congestive heart failure. Almost all these classes of antihyperglcyemic agents can be used in various combinations with one another as well as with different insulin regimens. This article shows the chemical structures and summarizes the mechanistic and therapeutic aspects of the five main classes of noninsulin glucose-lowering medications approved for use in patients with type 2 diabetes.

Do Gut Microbes Taste?

Gut microbiota has emerged as a major metabolically active organ with critical functions in both health and disease. The trillions of microorganisms hosted by the gastrointestinal tract are involved in numerous physiological and metabolic processes including modulation of appetite and regulation of energy in the host spanning from periphery to the brain. Indeed, bacteria and their metabolic byproducts are working in concert with the host chemosensory signaling pathways to affect both short- and long-term ingestive behavior. Sensing of nutrients and taste by specialized G protein-coupled receptor cells is important in transmitting food-related signals, optimizing nutrition as well as in prevention and treatment of several diseases, notably obesity, diabetes and associated metabolic disorders. Further, bacteria metabolites interact with specialized receptors cells expressed by gut epithelium leading to taste and appetite response changes to nutrients. This review describes recent advances on the role of gut bacteria in taste perception and functions. It further discusses how intestinal dysbiosis characteristic of several pathological conditions may alter and modulate taste preference and food consumption via changes in taste receptor expression.

Anti-Obesity Effect of Fermented Panax notoginseng Is Mediated Via Modulation of Appetite and Gut Microbial Population.

Panax notoginseng (PN) is a traditional herbal medicine containing several active compounds such as saponins and ginsenosides with many therapeutic applications including anti-obesity activity. Fermentation by lactic acid bacteria has the potential to metabolize ginsenosides to more active forms. This study examined whether fermentation has any benefits on the protective effects of a PN extract against obesity using a high-fat diet (HFD)-fed mouse model. PN was fermented with Lactobacillus plantarum which exhibited high β-glucosidase activity. Upon fermentation, the PN extract exhibited an altered ginsenoside profile, a dramatic increase in the lactate level. Treatment of the HFD group with fermented PN (FPN), but not PN, decreased both the food and calorie intake significantly, which was consistent with the more potent suppressing effects of FPN than PN on the signaling pathways involved in appetite and energy intake. The PN treatment also modulated the gut microbial composition. The PN and FPN treatment groups showed clear differences in the population of gut microbiota. The relative abundance of Bacteroidetes, Erysipelotrichaceae, Coprococus, and Dehalobacterium were significantly higher in the FPN group then the normal, HFD, and XEN groups. Furthermore, the relative abundances of Akkermansia, Dehalobacterium, Erysipeliotrichaceae and parpabacteroides were significantly higher in the FPN group than the PN group, but the relative abundances of Allobaculum, Erysipelotrichi and Erysipelotrichale were significantly lower. The relative abundance of Bacteroides and Lactococcus was significantly higher and lower, respectively in the PN and FPN groups than the HFD group. In conclusion, the altered ginsenoside and organic acid’s profile, and altered gut microbial composition are believed to be the major factors contributing to the anti-obesity properties of FPN.