Anti‐ApoA‐1 IgGs predict resistance to waist circumference reduction after Mediterranean diet

Carbone, Federico; Ciaula, Agostino Di; Pagano, Sabrina; Minetti, Silvia; Ansaldo, Anna Maria; Ferrara, Daniele; Belfiore, Anna; Elia, Edoardo; Pugliese, Stefania; Palmieri, Vincenzo; Montecucco, Fabrizio; Vuilleumier, Nicolas; Portincasa, Piero

doi:10.1111/eci.13410

Cited by 2 publications

(1 citation statement)

References 16 publications

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“…From a therapeutic perspective, if weight loss remains the cornerstone of NAFLD patient management, sodium-glucose cotransporter type-2 inhibitors (SGLT-2i) are emerging NAFLD therapeutic pharmacological molecules due to their ability to inhibit SREBP-1, hepatocyte inflammation, and liver fibrosis [43]. As AAA-1 have been shown to predict resistance to fat loss after dieting [44] and to predict reduced excess body mass index loss following bariatric surgery [45], and obviously act as antagonists of the beneficial properties of this class of pharmacological compounds, knowing if SGLT-2i could revert the pro-steatotic, and pro-inflammatory effects of AAA-1 is worth further study. Such investigations could validate or invalidate the hypothesis that AAA-1 assessment in NAFLD can be used to identify the subset of patients particularly likely to benefit from SGLT-2 inhibition.…”

Section: Discussionmentioning

confidence: 99%

Antibody against apolipoprotein-A1, non-alcoholic fatty liver disease and cardiovascular risk: a translational study

Pagano,

Bakker,

Juillard

et al. 2023

J Transl Med

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Background Non-alcoholic fatty liver disease (NAFLD) is a common liver disease increasing cardiovascular disease (CVD) morbidity and mortality. Autoantibodies against apolipoprotein A-1 (AAA-1) are a possible novel CVD risk factor promoting inflammation and disrupting cellular lipid homeostasis, two prominent pathogenic features of NAFLD. We explored the role of AAA-1 in NAFLD and their association with CVD risk. Methods HepaRG cells and liver sections from ApoE−/− mice exposed to AAA-1 were used for lipid quantification and conditional protein expression. Randomly selected sera from 312 subjects of the Prevention of Renal and Vascular End-stage Disease (PREVEND) general population cohort were used to measure AAA-1. A Fatty Liver Index (FLI) ≥ 60 and a 10-year Framingham Risk Score (FRS) ≥ 20% were used as proxy of NAFLD and high CVD risk, respectively. Results In-vitro and mouse models showed that AAA-1 increased triglyceride synthesis leading to steatosis, and promoted inflammation and hepatocyte injury. In the 112 PREVEND participants with FLI ≥ 60, AAA-1 were associated with higher FRS, alkaline phosphatase levels, lower HDL cholesterol and tended to display higher FLI values. Univariate linear and logistic regression analyses (LRA) confirmed significant associations between AAA-1, FLI and FRS ≥ 20%, while in adjusted LRA, FLI was the sole independent predictor of FRS ≥ 20% (OR: 1.05, 95%CI 1.01–1.09, P = 0.003). AAA-1 was not an independent FLI predictor. Conclusions AAA-1 induce a NAFLD-compatible phenotype in vitro and in mice. Intricate associations exist between AAA-1, CVD risk and FLI in the general population. Further work is required to refine the role of AAA-1 in NAFLD and to determine if the AAA-1 association with CVD is affected by hepatic steatosis.

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Section: Discussionmentioning

confidence: 99%

Antibody against apolipoprotein-A1, non-alcoholic fatty liver disease and cardiovascular risk: a translational study

Pagano,

Bakker,

Juillard

et al. 2023

J Transl Med

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The Potential of the Mediterranean Diet to Improve Mitochondrial Function in Experimental Models of Obesity and Metabolic Syndrome

et al. 2022

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The abnormal expansion of body fat paves the way for several metabolic abnormalities including overweight, obesity, and diabetes, which ultimately cluster under the umbrella of metabolic syndrome (MetS). Patients with MetS are at an increased risk of cardiovascular disease, morbidity, and mortality. The coexistence of distinct metabolic abnormalities is associated with the release of pro-inflammatory adipocytokines, as components of low-to-medium grade systemic inflammation and increased oxidative stress. Adopting healthy lifestyles, by using appropriate dietary regimens, contributes to the prevention and treatment of MetS. Metabolic abnormalities can influence the function and energetic capacity of mitochondria, as observed in many obesity-related cardio-metabolic disorders. There are preclinical studies both in cellular and animal models, as well as clinical studies, dealing with distinct nutrients of the Mediterranean diet (MD) and dysfunctional mitochondria in obesity and MetS. The term “Mitochondria nutrients” has been adopted in recent years, and it depicts the adequate nutrients to keep proper mitochondrial function. Different experimental models show that components of the MD, including polyphenols, plant-derived compounds, and polyunsaturated fatty acids, can improve mitochondrial metabolism, biogenesis, and antioxidant capacity. Such effects are valuable to counteract the mitochondrial dysfunction associated with obesity-related abnormalities and can represent the beneficial feature of polyphenols-enriched olive oil, vegetables, nuts, fish, and plant-based foods, as the main components of the MD. Thus, developing mitochondria-targeting nutrients and natural agents for MetS treatment and/or prevention is a logical strategy to decrease the burden of disease and medications at a later stage. In this comprehensive review, we discuss the effects of the MD and its bioactive components on improving mitochondrial structure and activity.

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Anti‐ApoA‐1 IgGs predict resistance to waist circumference reduction after Mediterranean diet

Cited by 2 publications

References 16 publications

Antibody against apolipoprotein-A1, non-alcoholic fatty liver disease and cardiovascular risk: a translational study

Antibody against apolipoprotein-A1, non-alcoholic fatty liver disease and cardiovascular risk: a translational study

The Potential of the Mediterranean Diet to Improve Mitochondrial Function in Experimental Models of Obesity and Metabolic Syndrome

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