Insulin signaling is a conserved pathway that orchestrates glucose and lipid metabolism, energy balance, and inflammation, and its dysregulation compromises the homeostasis of multiple systems. Insulin resistance is a shared hallmark of several metabolic diseases, including obesity, metabolic syndrome, and type 2 diabetes, and has been associated with cognitive decline during aging and dementia. Numerous mechanisms promoting the development of peripheral and central insulin resistance have been described, although most of them were not completely clarified. In the last decades, several studies have highlighted that biliverdin reductase-A (BVR-A), over its canonical role in the degradation of heme, acts as a regulator of insulin signaling. Evidence from human and animal studies show that BVR-A alterations are associated with the aberrant activation of insulin signaling, metabolic syndrome, liver steatosis, and visceral adipose tissue inflammation in obese and diabetic individuals. In addition, recent findings demonstrated that reduced BVR-A levels or impaired BVR-A activation contribute to the development of brain insulin resistance and metabolic alterations in Alzheimer's disease. In this narrative review, we will provide an overview on the literature by focusing on the role of BVR-A in the regulation of insulin signaling and how BVR-A alterations impact on cell dysfunctions in both metabolic and neurodegenerative disorders.

Role of biliverdin reductase A in the regulation of insulin signaling in metabolic and neurodegenerative diseases: An update / Cimini, FLAVIA AGATA; Perluigi, Marzia; Barchetta, Ilaria; Cavallo, Maria Gisella; Barone, Eugenio. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 23:10(2022), p. 5574. [10.3390/ijms23105574]

Role of biliverdin reductase A in the regulation of insulin signaling in metabolic and neurodegenerative diseases: An update

Flavia Agata Cimini;Marzia Perluigi;Ilaria Barchetta;maria gisella cavallo;Eugenio Barone
2022

Abstract

Insulin signaling is a conserved pathway that orchestrates glucose and lipid metabolism, energy balance, and inflammation, and its dysregulation compromises the homeostasis of multiple systems. Insulin resistance is a shared hallmark of several metabolic diseases, including obesity, metabolic syndrome, and type 2 diabetes, and has been associated with cognitive decline during aging and dementia. Numerous mechanisms promoting the development of peripheral and central insulin resistance have been described, although most of them were not completely clarified. In the last decades, several studies have highlighted that biliverdin reductase-A (BVR-A), over its canonical role in the degradation of heme, acts as a regulator of insulin signaling. Evidence from human and animal studies show that BVR-A alterations are associated with the aberrant activation of insulin signaling, metabolic syndrome, liver steatosis, and visceral adipose tissue inflammation in obese and diabetic individuals. In addition, recent findings demonstrated that reduced BVR-A levels or impaired BVR-A activation contribute to the development of brain insulin resistance and metabolic alterations in Alzheimer's disease. In this narrative review, we will provide an overview on the literature by focusing on the role of BVR-A in the regulation of insulin signaling and how BVR-A alterations impact on cell dysfunctions in both metabolic and neurodegenerative disorders.
2022
Alzheimer’s disease; biliverdin reductase A; dementia; insulin signaling; metabolic disorders; neurodegenerative diseases; obesity; type 2 diabetes; Animals; Inflammation; Insulin; Obesity; Oxidoreductases Acting on CH-CH Group Donors; Diabetes Mellitus, Type 2; Insulin Resistance; Metabolic Syndrome; Neurodegenerative Diseases
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Role of biliverdin reductase A in the regulation of insulin signaling in metabolic and neurodegenerative diseases: An update / Cimini, FLAVIA AGATA; Perluigi, Marzia; Barchetta, Ilaria; Cavallo, Maria Gisella; Barone, Eugenio. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 23:10(2022), p. 5574. [10.3390/ijms23105574]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1642699
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