Neurobiological and Microbiota Alterations After Bariatric Surgery: Implications for Hunger, Appetite, Taste, and Long-Term Metabolic Health

Abstract

Bariatric surgery (BS) is an effective intervention for obesity, inducing significant neurobiological and gut microbiota changes that influence hunger, appetite, taste perception, and long-term metabolic health. This narrative review examines these alterations by analyzing recent findings from clinical and preclinical studies, including neuroimaging, microbiome sequencing, and hormonal assessments. BS modulates appetite-regulating hormones, reducing ghrelin while increasing glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY), leading to enhanced satiety and decreased caloric intake. Neuroimaging studies reveal structural and functional changes in brain regions involved in reward processing and cognitive control, contributing to reduced cravings and altered food choices. Additionally, BS reshapes the gut microbiota, increasing beneficial species such as Akkermansia muciniphila, which influence metabolic pathways through short-chain fatty acid production and bile acid metabolism. These findings highlight the complex interplay between the gut and the brain in post-surgical metabolic regulation. Understanding these mechanisms is essential for optimizing post-operative care, including nutritional strategies and behavioral interventions. Future research should explore how these changes impact long-term outcomes, guiding the development of targeted therapies to enhance the recovery and quality of life for BS patients.

Keywords: GLP-1; appetite regulation; bariatric surgery; food cravings; ghrelin; gut–brain axis; hormonal changes; metabolic health; microbiota; short-chain fatty acid.

Figure 1

The figure depicts the progression of physiological and behavioral changes that occur after bariatric surgery (BS), including Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and laparoscopic adjustable gastric banding (LAGB). These surgical procedures alter the gastrointestinal (GI) tract, triggering remarkable changes in gut hormones (GLP-1 and PYY ↑, ghrelin ↓), bile acid modification, gut microbiota, and the amount of nutrient absorption. These modifications influence eating behavior by lowering appetite perception and energy intake and improving dietary adherence [82,90,100].

Figure 2

Changes in the microbiota after BS, with increased Akkermansia, decrease inflammation at peripheral and cerebral levels, influence the diversity of bile acids and metabolism of SCFAs, which exert their effect on enteroendocrine L-cell receptors with increased release of GLP-1 and PYY, which through vagal afferents alter neuronal activity modulating appetite and satiety. SCFAs: short-chain fatty acids; GLP-1: glucagon-like peptide-1; PYY: peptide tyrosine-tyrosine; ↑ increased; ↓ decreased [30,116,132,133].