Abstract
The prevention and treatment of obesity is primary based on the follow-up of a healthy lifestyle, which includes a healthy diet with an important presence of bioactive compounds such as polyphenols. For many years, the health benefits of polyphenols have been attributed to their anti-oxidant capacity as free radical scavengers. More recently it has been described that polyphenols activate other cell-signaling pathways that are not related to ROS production but rather involved in metabolic regulation. In this review, we have summarized the current knowledge in this field by focusing on the metabolic effects of flavonoids. Flavonoids are widely distributed in the plant kingdom where they are used for growing and defensing. They are structurally characterized by two benzene rings and a heterocyclic pyrone ring and based on the oxidation and saturation status of the heterocyclic ring flavonoids are grouped in seven different subclasses. The present work is focused on describing the molecular mechanisms underlying the metabolic impact of flavonoids in obesity and obesity-related diseases. We described the effects of each group of flavonoids in liver, white and brown adipose tissue and central nervous system and the metabolic and signaling pathways involved on them.
Highlights
Overnutrition and unhealthy diets together with physical inactivity cause an impairment in the metabolic homeostasis that lead to the development of pathologies such as obesity, type 2 diabetes, cardiovascular diseases (CVD) and more recently this kind of lifestyle has been linked to neuroinflammation and neurodegenerative diseases [1,2,3,4,5]
We have summarized the current knowledge on the metabolic effects of a specific group of polyphenols, the flavonoids, and the molecular mechanisms underlying these effects
Flavonoids are abundant in food and beverages highly consumed by human population including fruits, vegetables, tea, cocoa or wine [42] and in global are the bioactive compounds more largely associated with a reduced risk of all-cause mortality, type 2 diabetes [43,44,45,46], CVD [36,47], obesity and its comorbidities such as non-alcoholic fatty liver disease (NAFLD) [48,49,50] and more recently they have been described as potential therapeutic agents against cognitive pathologies such as Alzheimer’s disease (AD) [42,51,52] or cerebrovascular alterations [47]
Summary
Overnutrition and unhealthy diets together with physical inactivity cause an impairment in the metabolic homeostasis that lead to the development of pathologies such as obesity, type 2 diabetes, cardiovascular diseases (CVD) and more recently this kind of lifestyle has been linked to neuroinflammation and neurodegenerative diseases [1,2,3,4,5]. The metabolic syndrome (MetS) is the medical term used to define the concomitance in an individual of some of the following alterations: hyperglycemia and/or insulin resistance, arterial hypertension, dyslipidemia and central or abdominal obesity [6] It is currently one of the main public health problems worldwide and its incidence increases significantly each year, Nutrients 2020, 12, 2393; doi:10.3390/nu12082393 www.mdpi.com/journal/nutrients. Some evidences indicate that at some point, WAT fails to adequately keep the surplus of nutrients and together with an insufficient differentiation of new adipocytes lead to an off-WAT accumulation of lipids in peripheral relevant organs This ectopic accumulation of lipids causes lipotoxicity that may be, at least in part, responsible of the metabolic obesity-related metabolic dysfunctions [7]. Studies in humans and experimental approaches whit animal models from the last years have been included, avoiding cell culture experimental approaches except when relevant
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