Dietary fibers, and more specifically water-soluble fibers, beneficially affect human health. Guar gum and its enzymatic product, partially hydrolyzed guar gum (PHGG), are among the most studied dietary fibers in humans. Altogether, they can be described as "guar fiber". We performed a narrative review of the literature on guar fiber, namely guar gum and its partially hydrolyzed product, and their impact on human health, with a special focus on the gastrointestinal tract, gut microbiota, gut-brain axis, and liver steatosis. Accordingly, a literature search was conducted using the following keywords and combinations: guar fiber, guar gum, partially hydrolyzed guar gum, disorders of gut-brain interaction, gut-liver axis, and gut microbiota. Guar gum and its derivative, PHGG, show promising effects in gastrointestinal disorders, such as constipation and diarrhea. Interestingly, they can modulate the gut microbiota, with promising implications for the gut-brain axis and disorders of gut-brain interaction, such as irritable bowel syndrome. There are also interesting, albeit preliminary, results regarding their use in fatty liver disease. Thus, dietary fibers such as guar gum and, more importantly, its hydrolyzed product, show promising and better-documented effects on the health of the gastrointestinal tract and other organs and systems of the human body. However, the latter evidence still requires clinical confirmation of preclinical findings. Overall, the reviewed data vary in quality and maturity across different outcome domains.

Serotonin (5-hydroxytryptamine [5-HT]) is a key regulator of gastrointestinal function and exerts its effects through a diversity of 5-HT receptors. In the gut, 5-HT is released primarily by enterochromaffin cells, which act as specialized epithelial chemo- and mechanosensors. In humans, 5-HT modulates gastric sensorimotor function, and animal studies suggest that it is involved in enteric neurogenesis. Altered serotonergic signaling is increasingly recognized as an important contributor to the pathophysiology of gastric motility disorders and, therefore, represents an important therapeutic target. Although early serotonergic agents such as cisapride were withdrawn due to safety concerns, newer receptor-specific ligands have become available, broadening the therapeutic landscape and underscoring the need for an updated synthesis of serotonergic pathways and therapies in gastric motility disorders. For the management of gastroparesis, 5-HT4 agonists are the most consistently supported serotonergic agents in international guidelines, with evidence for improving gastric emptying and symptoms, and 5-HT3 antagonists are used primarily for symptomatic control of nausea and vomiting. In functional dyspepsia, serotonergic therapies may be selectively considered for off-label use based on the symptom profile, including mirtazapine (a 5-HT2 antagonist) in patients with early satiety and weight loss, and buspirone (a 5-HT1A agonist) in those with early satiety, postprandial fullness, or bloating. Although selective serotonin reuptake inhibitors and serotonin-noradrenaline reuptake inhibitors are not recommended for use in gastroparesis or functional dyspepsia, their potential role warrants further investigation, particularly given their established efficacy in conditions with chronic pain. Large, controlled trials evaluating the efficacy of serotonergic agents in gastroparesis and functional dyspepsia remain lacking, but recent developments highlight the continued relevance of serotonergic modulation. Recent data on naronapride, a newer 5-HT4 agonist, suggest that more selective agents may offer a clinically relevant benefit, while mitigating cardiovascular safety risks associated with earlier agents. By integrating molecular, physiological, and clinical data, this review aims to clarify the relevance of serotonergic signaling in gastric physiology and motility disorders, define its therapeutic applications, and identify the key remaining evidence gaps.

Central nervous system and peripheral clocks regulate the rhythms of life. Main zeitgebers are light-darkness, nutrition, and fasting cycles. There is a fine interaction among human body clocks, and different stimuli can affect and modulate biorhythms. Nutrition is one of these. Its role is still under investigation, especially in healthy status balance maintenance of critical and noncritical patients. For these reasons, a narrative review of the current literature on the definition of circadian clocks, their regulation, and the role of diet in their fine-tuning in critical and non-critical care patients was conducted. A search was conducted on PubMed and Medline for original articles, reviews, meta-analyses, and case series matching the following keywords and associations: enteral nutrition; circadian rhythms; chrononutrition; critically ill patient; personalized nutrition. A total of 1188 manuscripts were identified according to keywords. Subsequently, 579 articles were removed due to duplication, 208 due to non-English language, book chapter publications, and non-matching keyword combinations. The remaining 401 papers were checked for eligibility, and 170 manuscripts were accepted. Human central and peripheral circadian clocks are affected by several zeitgebers. Food micro- and macronutrients and time of administration can all affect peripheral clocks and interact with central ones. In critical and non-critical care patients, route and timing of artificial nutrition administration should consider the behaviour of different central and peripheral circadian clocks. This is also affected by inherited genetic biotypes. In detail, specific macronutrient patterns modulate peripheral clock gene expression and influence metabolic recovery in critically ill patients. In fact, timed and/or time-restricted setups of enteral nutrition administration (namely, timed enteral nutrition refers to administration according to circadian rhythms) show promising and yet incomplete data on their efficacy for restoring healthy status in the patients. Human circadian rhythms recognize nutrition as one of the main regulators. Both food composition and administration schemes can help to establish effective cycles in critical and non-critical admitted patients.

Postoperative complications in gastrointestinal (GI) cancer patients remain a significant challenge for physicians. It leads to increased morbidity, prolonged hospital stays, and higher healthcare costs. Enteral immunonutrition (EIN) has emerged as a promising add-on treatment to modulate immune response following surgery. In fact, it reduces inflammation and promotes patients’ recovery. Indeed, the literature data on its real clinical impact for the patients are inconsistent and, yet, poorly investigated. Thus, the aim of this review was to narratively assess the current evidence for the use of EIN in postoperative GI cancer patients, evaluating the effect on clinical and immunological outcomes of patients. Therefore, a literature search was conducted using the following keywords and associations: enteral immunonutrition, gastrointestinal cancer, immune response, inflammation, and postoperative complication. GI cancers, mainly esophageal and gastric cancer, represent a significant global health burden, characterized by high incidence and mortality rates. The complex interplay between tumor progression, systemic inflammation, and host nutritional status profoundly impacts patient outcomes. Traditional cancer treatments are effective and often lead to severe side effects. The latter includes malnutrition and immunosuppression and can significantly affect patients’ recovery. In recent times, the concept of immunonutrition has emerged as a promising add-on therapy able to consensually modulate immune response and improve nutritional status. Several studies and meta-analyses suggest that EIN can reduce postoperative infections (e.g., wound infections and sepsis incidence), shorten hospital stays, and improve overall outcomes in GI cancer surgery patients vs. standard enteral feeding. EIN is a promising add-on approach for the management of postoperative GI cancer patients. It can significantly reduce postoperative complications and enhance their recovery. However, the result seems consistent for gastric but not yet esophageal cancer patients. EIN shows high tolerance and a high safety profile.

The gastrointestinal tract plays a key role in the control of appetite and food intake through upper gastrointestinal secretomotor function and release of gut peptides. The therapeutic efficacy of glucagon-like peptide-1 receptor agonists in the treatment of obesity, type 2 diabetes and several other non-communicable diseases linked to the metabolic syndrome, have established the validity of gastrointestinal signals as a target for the regulation of food intake. This review summarizes recent and ongoing research on luminal and systemic approaches to control appetite and food intake by modulating gastrointestinal signals. These modalities include luminal delivery of specific nutrients and tastants to alter gut peptide secretion, influence gastric accommodation or alter the occurrence of interdigestive gastric phase 3. Comparable effects can be achieved by a number of classical pharmaceutical approaches. The majority of studies are limited to short-term studies in healthy controls. Larger scale long-term studies in patient cohorts are now needed to evaluate the efficacy of these modalities to control appetite and food intake.

Metabolic syndrome (MetS) is a complex and heterogeneous condition characterized by the coexistence of obesity, type 2 diabetes mellitus (T2DM), hypertension, chronic low-grade inflammation, and metabolic dysfunction. Increasing evidence suggests that the gut microbiota plays a central role in the development and progression of MetS by influencing host metabolism, intestinal barrier integrity, immune activation, endocrine signaling, and vascular homeostasis. This narrative review summarizes current evidence regarding gut microbiota alterations across major obesity-related metabolic phenotypes, including obesity alone, obesity complicated by T2DM, and obesity associated with hypertension. Obesity is generally characterized by reduced microbial diversity, depletion of beneficial taxa such as Faecalibacteriumprausnitzii and Akkermansia muciniphila, impaired short-chain fatty acid (SCFA) signaling, increased intestinal permeability, and metabolic endotoxemia. The coexistence of T2DM is associated with a more pronounced depletion of butyrate-producing bacteria, altered bile acid metabolism, impaired incretin signaling, and enhanced inflammatory activation that may contribute to insulin resistance and hyperglycemia. In hypertensive obesity, gut dysbiosis appears to preferentially involve disturbances within the gut-vascular axis, including reduced SCFA-producing taxa, increased trimethylamine N-oxide production, endothelial dysfunction, oxidative stress, and vascular inflammation. Although microbial signatures partially overlap among metabolic phenotypes, functional alterations in microbial metabolites and host-microbiota interactions may better explain disease heterogeneity than isolated taxonomic changes. Current evidence supports the potential role of microbiota-targeted interventions and integrated multi-omics approaches in future precision medicine strategies for cardiometabolic disease prevention and management.

Background: Critical illness is characterized by profound and rapidly evolving metabolic derangements driven by systemic inflammation, hypercatabolism, fluid shifts, and endocrine dysregulation. These dynamic changes markedly limit the accuracy of predictive equations, increasing the risk of both underfeeding and overfeeding. Indirect Calorimetry Energy represents the gold standard for measuring energy expenditure, while bioelectrical impedance vector analysis (BIVA) provides complementary insights into hydration status, cellular integrity, and body cell mass. In palliative care, AI-supported integration of indirect calorimetry and BIVA enables goal-concordant artificial nutrition by aligning energy delivery with real-time metabolic status while minimizing symptom burden. Artificial intelligence (AI) has emerged as a promising tool to integrate these heterogeneous data streams and support adaptive nutritional strategies. Methods: We conducted a structured narrative review of the literature published between 2000 and 2025 using PubMed, Scopus, Embase, and Web of Science. Artificial intelligence was not used to perform the literature search or study selection. Instead, AI was analyzed as a clinical and technological component within the included studies and explored as a future enabling strategy. Eligible publications involved adult critically ill patients and addressed indirect calorimetry, BIVA-derived parameters, or AI-based metabolic modeling applied to nutritional support. Given the heterogeneity of study designs and outcomes, findings were synthesized qualitatively. Results: Predictive equations showed substantial inaccuracy in unstable metabolic states, with errors frequently exceeding ±20-40%. Indirect calorimetry enabled individualized assessment of energy expenditure but remained limited by intermittent availability. Serial BIVA assessments consistently identified clinically relevant alterations in hydration status, body cell mass, and phase angle, the latter being strongly associated with adverse outcomes. Studies incorporating AI demonstrated improved integration of calorimetry, BIVA, and clinical variables, allowing identification of metabolic phenotypes, anticipation of metabolic shifts, and generation of adaptive nutritional recommendations. Conclusions: This narrative review highlights the complementary roles of Indirect Calorimetry and BIVA in characterizing metabolic needs in critical illness. Artificial intelligence does not replace these tools but enhances their clinical utility by integrating multidimensional data into dynamic, patient-specific nutritional strategies. The combined AI-IC-BIVA approach represents a promising framework for metabolic precision nutrition in the ICU, warranting prospective validation.

The transition from intensive care unit (ICU) to general wards marks a critical juncture in the recovery of critically ill patients, characterized by persistently high metabolic demands and vulnerability to malnutrition. Despite growing awareness of the importance of nutrition during this phase, there is a significant evidence gap regarding specific energy and protein requirements post-ICU discharge. This review explores the current recommendations and literature on energy and protein provision in ICU survivors, highlighting the complexity of post-ICU nutritional needs driven by hypermetabolism, physical rehabilitation, and the presence of anabolic resistance in older and frail patients. The inadequacy of nutritional intake in post-ICU settings is consistently reported, particularly among patients relying solely on oral nutrition. Barriers such as appetite dysregulation, dysphagia, post-intensive care syndrome, and systemic issues including rigid food service structures further compromise recovery. Innovative strategies, including the use of indirect calorimetry, targeted supplementation, and personalized nutritional interventions, are essential to bridge this “nutritional gap.” This review underscores the need for structured post-ICU nutritional care pathways, interdisciplinary coordination, and continued research to define evidence-based targets for energy and protein intake during convalescence.

Background and Objectives: Fatty Liver Disease is a major health problem worldwide. We can distinguish liver steatosis as non-associated or associated with chronic/acute alcohol consumption. These two entities share similar stages ranging from hepatic fat storage (namely, steatosis) to inflammation, necrosis, and fibrosis until hepatocellular carcinoma (HCC). Over time, “Metabolic Associated Fatty Liver Disease” (MAFLD) has replaced nonalcoholic fatty liver disease (NAFLD) nomenclature and has included cardiometabolic criteria in these patients definition. Thus, obesity, type 2 diabetes mellitus (T2DM), hypertension, and dyslipidemia are MAFLD features and are of the metabolic syndrome. Importantly, there is not a specific treatment for MAFLD, but there are therapeutic strategies that act on metabolic dysfunction related to MAFLD. They can reduce the progression of liver fibrosis and its complications. Materials and Methods: For all these reasons, we conducted a narrative review of the literature, and we focused on metabolic dysfunction related to MAFLD, with a special regard for cholesterol metabolism. Results: MAFLD is a recently redefined condition that better describes the metabolism derangement responsible for fatty liver disease. This distinguishes MAFLD from NAFLD. In fact, the diagnostic criteria for MAFLD require the presence of liver steatosis together with at least one of the following: obesity, T2DM, or evidence of metabolic disorder such as hypertriglyceridemia, low high-density lipoprotein cholesterol, or hypertension. As a result, MAFLD is closely linked to an increased cardiometabolic risk. Current therapeutic approaches can be used to reduce this risk, focusing on lifestyle interventions and pharmacological strategies. Several treatments in patients diagnosed with MAFLD are mainly cholesterol-lowering remedies. Among these, Pro-protein Convertase Subtilisin/Kexin type 9 inhibitors (PCSK9i) show the most promising efficacy profile but data on liver fibrosis are lacking. Agonists of GLP-1 receptor, Sodium-glucose cotransporter-2 inhibitors (SGLT2i) and Dipeptidyl Peptidase-4 inhibitors (DPP-4i) have a “ multi-hit “ action allowing their use also in diabetic patients with MAFLD. Conclusions: Lifestyle modifications, some nutraceuticals, statins, incretins, and PCSK9i have changed the natural course and significantly improved the cardiometabolic outcomes of MAFLD. Emerging cholesterol-lowering drugs, such as Bempedoic acid, can overcome low compliance to statins’ use and their controversial effect on liver fibrosis. Finally, medications targeting insulin resistance allow for strategic interventions of the convoluted pathophysiology of MAFLD in multiple steps, with the potential to reduce liver steatosis, inflammation, and necrosis and, sometimes even to reverse liver fibrosis.

Background: Malnutrition and muscle weakness are highly prevalent in critically admitted patients. To overcome sarcopenia and muscle weakness, physical activity and neuromuscular electric stimulation have been introduced with limited efficacy. Thus, several anabolic remedies have been introduced. An adequate increase in protein support according to indirect calorimetry and body composition and methyl hydroxybutyrate (HMB) is emerging. Therefore, we wanted to investigate the impact of HMB-enriched whey formula on the nutritional status, muscle weakness, and clinical course of critically ill patients undergoing nutritional status multimodal assessment and physical rehabilitation. Methods: We consecutively enrolled critically ill adult patients admitted to the intensive care unit (ICU) of “Santa Maria Hospital”, Terni, Italy. All patients underwent preliminary anthropometric, laboratory tests, nutritional (bioimpedance vector analysis and indirect calorimetry), and ultrasound muscle assessment at admission (T0). Laboratory tests monitoring continued throughout the ICU stay. Nutritional and muscle strength assessment was taken weekly throughout the patient’s ICU stay. All patients were enterally administered with a whey protein-enriched formula. Ten days after admission (during the physical rehabilitation period), patients were randomly administered a mixture of essential amino acids and methyl hydroxybutyrate (HMB). Results: We consecutively enrolled 54 ICU patients. At the baseline, survivors (n = 46) were significantly younger than non-survivors. The latter had a worse SAPS II score, nutritional status, and risk, with no significant difference in basal metabolism. Prealbumin values significantly correlated with improved nutritional status and metabolism. Starting from 10 days upon ICU admission, the pennation angle (used as a measure of muscle strength) significantly correlated with the improvement in nutritional status. Whey proteins were well tolerated. Its administration showed a tendency to improve the pennation angle. No specific effect of the mixture containing essential amino acids and methyl hydroxybutyrate was observed. Nutritional status improvement and the rise of basal metabolism were significantly correlated with the extubation time. On the other hand, the reduction in muscle weakness was not significantly correlated with the timing of extubation. Conclusions: Whey protein formula administration can significantly improve nutritional status and basal metabolism in ICU patients. This is reflected in improved muscle strength. Whey protein administration shows a tendency toward a rise in pennation angle. A similar and non-specific trend was observed upon HMB mixture add-one. Further prospective large-scale controlled studies are needed to confirm these promising results.

Background: There is limited knowledge about nutritional intake and energy needs during the post-intensive care unit (ICU) period and their relationship with clinical outcomes and physical recovery. Aims and Methods: Thus, this observational multicenter study (Azienda Ospedaliero-Universitaria “Santa Maria”, Terni and “Madonna del Soccorso” General hospital, San Benedetto del Tronto, Italy) aimed, firstly, to measure energy expenditure via indirect calorimetry (IC) (Q-NRG+® Metabolic Monitor, Cosmed, Rome, Italy), derived respiratory quotient (R/Q1) and, malnutrition risk via Mini Nutritional Assessment (MNA) test and body composition through bioimpedance vector analysis (BIVA-Akern, Pontassieve, Italy); secondly, to assess their effect on energy needs, body composition and physical rehabilitation steps in critically ill adults after ICU discharge. The provision of nutrients (PIS test) was also recorded. Oral nutritional supplementation was used to reach the optimal nutritional intake. All patients followed a standardized rehabilitation program. Results: A total of 43 patients were enrolled from January 2024 until February 2025 at the beginning of their post-ICU period. The mean age was 65.7 ± 1.0 years, the mean BMI was 20.73 ± 0.8 kg/m2 at the recovery ward, and 60.4% (n = 26) were male. The mean admission period was 19.5 ± 1.7 days. The resting energy expenditure (mREE) was 1591 ± 71.2 at the admission and 1.856 ± 62.7 kcal/kg/d at the discharge (p < 0.05). The median phase angle value was 4.33 ± 0.15 at the admission and 5.05 ± 0.17° at the discharge (p < 0.05); R/Q1 at the admission was 0.7 ± 0.1 and 1.086± 0.11 at the discharge (p < 0.05). Improved energy expenditure significantly correlated with R/Q1 and phase angle (r = 0.81 and r = 0.72, respectively). Interestingly, there was no significant correlation between improved metabolism and improved PIS test scores (r = 0.18). Improved metabolism and nutritional status showed a tendency to correlate with shorter post-ICU courses and earlier physical recovery, without reaching statistical significance. Conclusions: Measurement of energy expenditure and caloric intake, along with the assessment of body composition is feasible and provides an objective tool to guide and possibly enhance the functional recovery in patients during the post-ICU period.

Obesity has become one of modern society's most serious health problems. Studies from the last 30 years revealed a direct relationship between imbalanced energy intake and increased healthcare costs related to the treatment or management of obesity. Recent research has highlighted significant effects of gut microbial composition on obesity. We aimed to report the current knowledge on the definition, composition, and functions of intestinal microbiota. We have performed an extensive review of the literature searching for the following key words: metabolism, gut microbiota, dysbiosis, and obesity. There is evidence that an association between intestinal microbiota and obesity exists at any age. There are complex genetic, metabolic, and inflammatory mechanisms involved in the pathogenesis of obesity. Revision of indications for use of probiotics, prebiotics, and antibiotics in obese patients should be considered. Microbial composition of the gut may be an important factor involved in the development of obesity. Changes in the gut microbiota may result in changes in human metabolism and weight loss.

Gastric cancer (GC) is one of the most common causes of cancer deaths, and GC treatments represent a large area of research. Although initially regarded as a sterile organ and unsuitable for microbial communities, the discovery of Helicobacter pylori made us realize that some microbes can colonize the stomach. In recent years, growing interest in gastric bacteria has expanded to the gut microbiota and, more recently, to the oral microbiota. Indeed, the oral–gastric–gut microbiota axis may play a crucial role in maintaining homeostasis, while changes in microbiota composition in GC patients can influence clinical outcomes. On the one hand, the microbiota and its metabolites may significantly influence the progression of GC, while anti-GC treatments such as gastrectomy and chemotherapy may significantly impact the oral–gastric–gut microbiota axis of GC patients. In this context, the role of nutritional therapies, including diet, prebiotics, and probiotics, in treating GC should not be underestimated. Wit this review, we aim to highlight the main role of the gastric, oral, and gut microbiota in GC onset and progression, representing potential future biomarkers for early GC detection and a target for efficient nutritional therapies during the course of GC.

Background: Disorders of gut–brain interaction (DGBIs) have a complex pathophysiology that is often characterized by a relationship between food ingestion and triggering of symptoms. Understanding of the underlying mechanisms and the role of nutrients as a therapeutic target are rapidly evolving. Aims and methods: We performed a narrative review of the literature using the following keywords, their acronyms, and their associations: nutrients, disorders of gut–brain interaction; functional dyspepsia; malabsorption; irritable bowel syndrome; diarrhea; constipation. Results: Functional dyspepsia displayed a significant correlation between volume, fat and/or wheat abundance, chemical composition of ingested food and symptoms of early satiety, fullness and weight loss. Carbohydrate malabsorption is related to enzyme deficiency throughout the GI tract. Food composition and richness in soluble vs. non-soluble fibers is related to constipation and diarrhea. The elimination of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) has a significant and non-unidirectional impact on irritable bowel syndrome (IBS) symptoms. Conclusions: Food volume, nutritive and chemical composition, and its malabsorption are associated with symptom generation in DGBIs. Further multicenter, randomized-controlled clinical trials are needed to clarify the underlying pathophysiology.

BACKGROUND AND AIM:Antimicrobial resistance (AMR) is a chronic issue of our Westernized society, mainly because of the uncontrolled and improper use of antimicrobials. The coronavirus disease 2019 (COVID-19) pandemic has triggered and expanded AMR diffusion all over the world, and its clinical and therapeutic features have changed. Thus, we aimed to review evidence from the literature on the definition and causative agents of AMR in the frame of the COVID-19 post-pandemic era.METHODS:We conducted a search on PubMed and Medline for original articles, reviews, meta-analyses, and case series using the following keywords, their acronyms, and their associations: antibiotics, antimicrobial resistance, severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), COVID-19 pandemic, personal protective equipment.RESULTS:AMR had a significant rise in incidence both in in-hospital and outpatient populations (ranging from 5 up to 50%) worldwide, but with a variegated profile according to the germ and microorganism considered. Not only bacteria but also fungi have developed more frequent and diffuse AMR. These findings are explained by the increased use and misuse of antibiotics and preventive measures during the first waves of the SARS-CoV2 pandemic, especially in hospitalized patients. Subsequently, the reduction in and end of the lockdown and the use of personal protective equipment have allowed for the indiscriminate circulation of resistant microorganisms from low-income countries to the rest of the world with the emergence of new multi- and polyresistant organisms. However, there is not a clear association between COVID-19 and AMR changes in the post-pandemic period.CONCLUSIONS:AMR in some microorganisms has significantly increased and changed its characteristics during and after the end of the pandemic phase of COVID-19. An integrated supranational monitoring approach to this challenge is warranted in the years to come. In detail, a rational, personalized, and regulated use of antibiotics and antimicrobials is needed.

BACKGROUND:Dumping syndrome is a complex of gastrointestinal symptoms originally studied in peptic ulcer surgery patients. At present, it is most prevalent in patients who underwent bariatric, upper gastrointestinal cancer or anti-reflux surgery. The symptom pattern comprises early and late dumping symptoms. Several management options have been reported including nutritional, pharmacological and surgical approaches. AIMS AND METHODS:In this study, we aimed to review the current evidence on dumping syndrome definition, diagnosis and treatment, including preliminary data from newer pharmacological studies. RESULTS:Current pathophysiological concepts and analyses of provocative tests has led to a clear definition of dumping syndrome, including both early and late dumping symptoms. The term postbariatric hypoglycemia represents a limited focus on late dumping only. The diagnosis relies on recognition of symptoms and signs in a patient with appropriate surgical history; and can be confirmed by provocative testing or registration of spontaneous hypoglycemia. The initial treatment focuses on dietary intervention, to which meal viscosity enhancers and/or the glycosidase inhibitor acarbose can be added. The most effective therapy is the use of short- or long-acting somatostatin analogues, which is however expensive and entails side effect issues. In case of refractory hypoglycemia, diazoxide or SGLT2 inhibitors can be considered, based on limited evidence. In refractory patients, continuous enteral feeding or (rarely) surgical reinterventions have been advocated, although not supported by solid evidence. Therapies under current evaluation include the broad-spectrum somatostatin analogue pasireotide, GLP-1 receptor antagonists, GLP-1 receptor agonists and administration of stable forms of glucagon are currently under study. CONCLUSIONS:Dumping syndrome is a well-defined but probably under-diagnosed complication of upper gastrointestinal, especially bariatric, and surgeries. Diagnosis is confirmed by a provocative test and incremental therapies starting with diet, adding meal viscosity enhancers or glycosidase inhibitors and adding somatostatin analogues in refractory cases. A number of emerging therapies targeting intestinal propulsion, peptide hormone effects and hypoglycemic events are under evaluation.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. This term does not describe the pathogenetic mechanisms and complications associated with NAFLD. The new definition, Metabolic Dysfunction-associated Steatotic Liver disease (MASLD), emphasizes the relationship between NAFLD and cardiometabolic comorbidities. Cardiovascular disease features, such as arterial hypertension and atherosclerosis, are frequently associated with patients with MASLD. Furthermore, these patients have a high risk of developing neoplastic diseases, primarily hepatocellular carcinoma, but also extrahepatic tumors, such as esophageal, gastric, and pancreatic cancers. Moreover, several studies showed the correlation between MASLD and endocrine disease. The imbalance of the gut microbiota, systemic inflammation, obesity, and insulin resistance play a key role in the development of these complications. This narrative review aims to clarify the evolution from NAFLD to the new nomenclature MASLD and evaluate its complications.