Long-term high-fat diet (HFD) consumption can cause weight gain and obesity, two conditions often associated with hepatic non-alcoholic fatty liver and oxidative stress. Oleoylethanolamide (OEA), a lipid compound produced by the intestine from oleic acid, has been associated with different beneficial effects in diet-induced obesity and hepatic steatosis. However, the role of OEA on hepatic oxidative stress has not been fully elucidated. In this study, we used a model of diet-induced obesity to study the possible antioxidant effect of OEA in the liver. In this model rats with free access to an HFD for 77 days developed obesity, steatosis, and hepatic oxidative stress, as compared to rats consuming a low-fat diet for the same period. Several parameters associated with oxidative stress were then measured after two weeks of OEA administration to diet-induced obese rats. We showed that OEA reduced, compared to HFD-fed rats, obesity, steatosis, and the plasma level of triacylglycerols and transaminases. Moreover, OEA decreased the amount of malondialdehyde and carbonylated proteins and restored the activity of antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, which decreased in the liver of HFD-fed rats. OEA had also an improving effect on parameters linked to endoplasmic reticulum stress, thus demonstrating a role in the homeostatic control of protein folding. Finally, we reported that OEA differently regulated the expression of two transcription factors involved in the control of lipid metabolism and antioxidant genes, namely nuclear factor erythroid-derived 2-related factor 1 (Nrf1) and Nrf2, thus suggesting, for the first time, new targets of the protective effect of OEA in the liver.

Unresolved inflammation represents a central feature of different human pathologies including neuropsychiatric, cardiovascular, and metabolic diseases. The epidemiologic relevance of such disorders justifies the increasing interest in further understanding the mechanisms underpinning the inflammatory process occurring in such chronic diseases to provide potential novel pharmacological approaches. The most common and effective therapies for controlling inflammation are glucocorticoids; however, a variety of other molecules have been demonstrated to have an anti-inflammatory potential, including neuropeptides. In recent years, the oxytocinergic system has seen an explosion of scientific studies, demonstrating its potential to contribute to a variety of physiological processes including inflammation. Therefore, the aim of the present review was to understand the role of oxytocin in the modulation of inflammation occurring in different chronic diseases. The criterion we used to select the diseases was based on the emerging literature showing a putative involvement of the oxytocinergic system in inflammatory processes in a variety of pathologies including neurological, gastrointestinal and cardiovascular disorders, diabetes and obesity. The evidence reviewed here supports a beneficial role of oxytocin in the control of both peripheral and central inflammatory response happening in the aforementioned pathologies. Although future studies are necessary to elucidate the mechanistic details underlying such regulation, this review supports the idea that the modulation of the endogenous oxytocinergic system might represent a new potential pharmacological approach for the treatment of inflammation.

Over the last few years considerable attention has been devoted to biological fluidized-bed technology which seems to be potentially more advantageous than both dispersed biomass processes and fixed bed systems. An obstacle to the spreading of this technology is the lack of rigorous criteria in designing reactors, due to the poor knowledge of interconnections of fluid-dynamic aspects with kinetic ones. This paper reviews the rational basis for reactor design and reports on the experimental tests carried out in order to gain a better understanding in the areas of biofilm modelling and fluidization mechanics. In particular a biofilm model, in the general case of the Michaelis and Menten equation, was developed and its validity was verified utilizing experimental data obtained in nitrifying batch tests. As to fluidization mechanics the experimental work confirms the Wen and Yu(1966) approach to correlate the bed porosity with the superficial liquid velocity.

Feeding is an intrinsic and fundamental behavior regulated by complex neurobiological networks that integrate peripheral metabolic signals with neurotransmitter systems within key brain regions. Histamine, a biogenic amine acting as a neuromodulator in the central nervous system, plays a crucial role in the regulation of food intake and energy homeostasis. Within the hypothalamus, histaminergic neurons influence appetite-related circuits, primarily through H₁R and H₃R. Central administration of histamine suppresses food consumption, an effect largely mediated via H₁R. The blockade of H₁R has been associated with increased appetite and weight gain, as observed with certain antihistaminic and antipsychotic drugs. Conversely, H₃R antagonists, which enhance histaminergic tone by preventing autoinhibition, exhibit anorexigenic properties. Histamine also modulates peripheral mechanisms such as gluconeogenesis and ketone body production. Clinically, pharmacological modulation of histaminergic receptors has gained interest as a potential therapeutic approach for treating obesity and related metabolic disorders. Promising results are emerging from clinical trials evaluating the efficacy of betahistine, a drug with a dual pharmacological profile as a weak H₁R agonist and potent H₃R antagonist, in restoring histaminergic tone and counteracting weight gain and metabolic side effects induced by antipsychotic therapies. Reduced H₁R binding in certain brain areas has been observed in patients with anorexia nervosa. In this review, we surveyed the role of brain histamine in the control of eating behavior and energy expenditure. We also described the implications of histamine release in the gut-brain axis and discussed available clinical data regarding the efficacy of histaminergic compounds in eating-related disorders.

The global burden of obesity continues to rise, demanding effective pharmacological strategies for individuals in whom prevention alone is insufficient. Recent incretin‐based and multi‐agonist therapies have delivered unprecedented weight loss, demonstrating that the simultaneous modulation of multiple metabolic pathways can optimize body weight control and improve obesity‐related comorbidities. However, biological heterogeneity, interindividual variability in treatment response and uncertainties regarding long‐term outcomes highlight the need to explore complementary regulatory mechanisms. Oleoylethanolamide (OEA) is an endogenous lipid mediator synthesized on demand in the small intestine in response to dietary lipid intake. Acting primarily through peroxisome proliferator‐activated receptor‐α (PPAR‐α), OEA functions as a physiological satiety signal that promotes fatty acid oxidation and coordinates gut–brain communication. Preclinical evidence indicates that OEA reduces food intake without inducing malaise, enhances lipid utilization and improves metabolic dysfunction in models of diet‐induced obesity, while engaging both homeostatic and reward‐related neural circuits. Emerging clinical studies report modest but consistent effects on body weight and selected cardiometabolic parameters. In this review, we summarize the current evidence on OEA biosynthesis, molecular targets and mechanisms of action, with particular focus on its role in the regulation of feeding behaviour, metabolic homeostasis and obesity‐related comorbidities, and discuss its potential positioning within the evolving landscape of anti‐obesity pharmacotherapy.

The global burden of obesity continues to rise, demanding effective pharmacological strategies for individuals in whom prevention alone is insufficient. Recent incretin-based and multi-agonist therapies have delivered unprecedented weight loss, demonstrating that the simultaneous modulation of multiple metabolic pathways can optimize body weight control and improve obesity-related comorbidities. Yet the biological heterogeneity of obesity, interindividual variability in treatment response, and uncertainties regarding long-term outcomes highlight the need to explore complementary mechanisms and diversify therapeutic options. Oleoylethanolamide (OEA) is an endogenous lipid mediator synthesized on demand by enterocytes from membrane phospholipids in response to dietary lipid intake. Acting primarily through peroxisome proliferator-activated receptor-α (PPAR-α), endogenous OEA functions as a physiological postprandial satiety signal that promotes fatty acid oxidation and coordinates gut–brain communication. Disruption of this pathway-through genetic or dietary manipulations-impairs metabolic homeostasis, underscoring its regulatory role. Pharmacological administration of OEA in preclinical models reduces food intake without inducing malaise, enhances lipid utilization, and ameliorates diet-induced metabolic dysfunction, while recruiting central circuits governing both homeostatic and reward-driven feeding. Early clinical studies report modest but consistent improvements in body weight and selected cardiometabolic markers, although limited trial size and duration preclude definitive conclusions. Clarifying pharmacokinetics, brain exposure, responder phenotypes, and rational combinations with incretin-based therapies will be essential to define OEA’s place within a more personalized and physiologically grounded anti-obesity therapeutic framework.