Could Naringenin Participate as a Regulator of Obesity and Satiety?
Gabriela López-AlmadaJesús Abraham Domínguez-AvilaMejía-León María EstherMaribel Robles-SánchezGustavo Adolfo González-AguilarNorma Julieta Salazar-LópezPublished in: Molecules (Basel, Switzerland) (2023)
Obesity is a serious health problem worldwide, since it is associated with multiple metabolic disorders and complications such as cardiovascular disease, type 2 diabetes, fatty liver disease and overall metabolic dysfunction. Dysregulation of the hunger-satiety pathway, which includes alterations of central and peripheral signaling, explains some forms of obesity by favoring hyperphagia and weight gain. The present work comprehensively summarizes the mechanisms by which naringenin (NAR), a predominant flavanone in citrus fruits, could modulate the main pathways associated with the development of obesity and some of its comorbidities, such as oxidative stress (OS), inflammation, insulin resistance (IR) and dyslipidemia, as well as the role of NAR in modulating the secretion of enterohormones of the satiety pathway and its possible antiobesogenic effect. The results of multiple in vitro and in vivo studies have shown that NAR has various potentially modulatory biological effects against obesity by countering IR, inflammation, OS, macrophage infiltration, dyslipidemia, hepatic steatosis, and adipose deposition. Likewise, NAR is capable of modulating peptides or peripheral hormones directly associated with the hunger-satiety pathway, such as ghrelin, cholecystokinin, insulin, adiponectin and leptin. The evidence supports the use of NAR as a promising alternative to prevent overweight and obesity.
Keyphrases
- insulin resistance
- type diabetes
- weight gain
- metabolic syndrome
- oxidative stress
- high fat diet induced
- adipose tissue
- weight loss
- cardiovascular disease
- high fat diet
- body mass index
- skeletal muscle
- polycystic ovary syndrome
- glycemic control
- birth weight
- healthcare
- mental health
- signaling pathway
- transcription factor
- dna damage
- physical activity
- heat stress
- coronary artery disease
- risk assessment
- climate change
- endoplasmic reticulum stress
- preterm birth
- social media
- chemotherapy induced