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  1. Article ; Online: Role of Glucocorticoids in Metabolic Dysfunction-Associated Steatotic Liver Disease.

    Polyzos, Stergios A / Targher, Giovanni

    Current obesity reports

    2024  

    Abstract: Purpose of the review: To summarize published data on the association between glucocorticoids and metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on the possible pathophysiological links and related treatment considerations.!## ...

    Abstract Purpose of the review: To summarize published data on the association between glucocorticoids and metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on the possible pathophysiological links and related treatment considerations.
    Recent findings: Glucocorticoids, commonly used for managing many inflammatory and autoimmune diseases, may contribute to the development and progression of MASLD. Glucocorticoids may induce hyperglycemia and hyperinsulinemia, thus increasing systemic and hepatic insulin resistance, a hallmark of MASLD pathogenesis. Furthermore, glucocorticoids increase adipose tissue lipolysis, and hepatic de novo lipogenesis and decrease hepatic fatty acid β-oxidation, thus promoting MASLD development. Preclinical evidence also suggests that glucocorticoids may adversely affect hepatic inflammation and fibrosis. 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and 5α-reductase are implicated in the link between glucocorticoids and MASLD, the former enzyme increasing and the latter reducing the glucocorticoid action on the liver. Treatment considerations exist due to the pathogenic link between glucocorticoids and MASLD. Since iatrogenic hypercortisolism is common, glucocorticoids should be used at the minimum daily dose to control the subjective disease. Furthermore, the pharmacologic inhibition of 11β-HSD1 has provided favorable results in MASLD, both in preclinical studies and early MASH clinical trials. Glucocorticoids are closely linked to MASLD pathophysiology, with specific clinical and therapeutic implications.
    Language English
    Publishing date 2024-03-08
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2162-4968
    ISSN (online) 2162-4968
    DOI 10.1007/s13679-024-00556-1
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  2. Article ; Online: Metabolic dysfunction-associated steatotic liver disease: Recent turning points for its diagnosis and management.

    Polyzos, Stergios A / Mantzoros, Christos S

    Metabolism: clinical and experimental

    2024  , Page(s) 155936

    Language English
    Publishing date 2024-05-17
    Publishing country United States
    Document type Editorial
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2024.155936
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  3. Article ; Online: Menopause and metabolic dysfunction-associated steatotic liver disease.

    Polyzos, Stergios A / Goulis, Dimitrios G

    Maturitas

    2024  , Page(s) 108024

    Abstract: Nonalcoholic fatty liver disease, recently proposed to be renamed metabolic dysfunction-associated steatotic liver disease, is a highly prevalent disease (25-30 % of the global general population) whose prevalence increases after menopause. Apart from ... ...

    Abstract Nonalcoholic fatty liver disease, recently proposed to be renamed metabolic dysfunction-associated steatotic liver disease, is a highly prevalent disease (25-30 % of the global general population) whose prevalence increases after menopause. Apart from the rates of simple steatosis, the severity of the disease (e.g., hepatic fibrosis) increases after menopause. Menopause is associated with higher abdominal adiposity and dysmetabolism of carbohydrate and lipid metabolism, which may contribute to the development and severity of metabolic dysfunction-associated steatotic liver disease and the higher cardiovascular risk observed after menopause. The association between menopause and metabolic dysfunction-associated steatotic liver disease renders menopausal hormone therapy an appealing way to reverse hepatic disease in parallel with the benefits of menopausal hormone therapy in other tissues. In this regard, most animal studies have shown a beneficial effect of estrogens on metabolic dysfunction-associated steatotic liver disease. Still, clinical studies are few, and their data are conflicting. The effect of menopausal hormone therapy on metabolic dysfunction-associated steatotic liver disease may be distinct among estrogen monotherapies and the combinations of estrogens and progestogens. It may also depend on the type of progestogen and the route of administration. However, more studies specifically designed for these aims are needed to draw secure conclusions. This review summarizes the data related to the association between menopause and metabolic dysfunction-associated steatotic liver disease, as well as between menopausal hormone therapy and metabolic dysfunction-associated steatotic liver disease, with a special focus on clinical studies.
    Language English
    Publishing date 2024-05-14
    Publishing country Ireland
    Document type Journal Article ; Review
    ZDB-ID 80460-5
    ISSN 1873-4111 ; 0378-5122
    ISSN (online) 1873-4111
    ISSN 0378-5122
    DOI 10.1016/j.maturitas.2024.108024
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  4. Article ; Online: Nonalcoholic Fatty Liver Disease and

    Polyzos, Stergios A / Kountouras, Jannis

    Current vascular pharmacology

    2023  Volume 21, Issue 2, Page(s) 78–80

    MeSH term(s) Humans ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/epidemiology ; Helicobacter pylori ; Helicobacter Infections/complications ; Helicobacter Infections/diagnosis ; Helicobacter Infections/drug therapy ; Risk Factors ; Liver
    Language English
    Publishing date 2023-02-08
    Publishing country United Arab Emirates
    Document type Editorial
    ZDB-ID 2192362-0
    ISSN 1875-6212 ; 1570-1611
    ISSN (online) 1875-6212
    ISSN 1570-1611
    DOI 10.2174/1570161121666230209161617
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  5. Article ; Online: Sarcopenia: still in relative definition-penia and severe treatment-penia.

    Polyzos, Stergios A / Mantzoros, Christos S

    Metabolism: clinical and experimental

    2023  Volume 150, Page(s) 155717

    MeSH term(s) Humans ; Sarcopenia/therapy ; Muscle Strength ; Muscle, Skeletal/pathology ; Hand Strength
    Language English
    Publishing date 2023-11-03
    Publishing country United States
    Document type Editorial
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2023.155717
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  6. Article ; Online: The Role of Tumor Necrosis Factor-Alpha in the Pathogenesis and Treatment of Nonalcoholic Fatty Liver Disease.

    Vachliotis, Ilias D / Polyzos, Stergios A

    Current obesity reports

    2023  Volume 12, Issue 3, Page(s) 191–206

    Abstract: Purpose of review: To summarize experimental and clinical evidence on the association between tumor necrosis factor-α (TNF-α) and nonalcoholic fatty liver disease (NAFLD) and discuss potential treatment considerations.: Recent findings: Experimental ... ...

    Abstract Purpose of review: To summarize experimental and clinical evidence on the association between tumor necrosis factor-α (TNF-α) and nonalcoholic fatty liver disease (NAFLD) and discuss potential treatment considerations.
    Recent findings: Experimental evidence suggests that TNF-α is a cytokine with a critical role in the pathogenesis of NAFLD. Although, the production of TNF-α may be an early event during the course of nonalcoholic fatty liver (NAFL), TNF-α may play a more substantial role in the pathogenesis of nonalcoholic steatohepatitis (NASH) and NAFLD-associated fibrosis. Moreover, TNF-α may potentiate hepatic insulin resistance, thus interconnecting inflammatory with metabolic signals and possibly contributing to the development of NAFLD-related comorbidities, including cardiovascular disease, hepatocellular carcinoma, and extra-hepatic malignancies. In clinical terms, TNF-α is probably associated with the severity of NAFLD; circulating TNF-α gradually increases from controls to patients with NAFL, and then, to patients with NASH. Given this potential association, various therapeutic interventions (obeticholic acid, peroxisome proliferator-activated receptors, sodium-glucose co-transporter 2 inhibitors, glucagon-like peptide-1 receptor agonists, probiotics, synbiotics, rifaximin, vitamin E, pentoxifylline, ursodeoxycholic acid, fibroblast growth factor-21, n-3 polyunsaturated fatty acids, statins, angiotensin receptor blockers) have been evaluated for their effect on TNF-α and NAFLD. Interestingly, anti-TNF biologics have shown favorable metabolic and hepatic effects, which may open a possible therapeutic window for the management of advanced NAFLD. The potential key pathogenic role of TNF-α in NAFLD warrants further investigation and may have important diagnostic and therapeutic implications.
    MeSH term(s) Humans ; Non-alcoholic Fatty Liver Disease/metabolism ; Tumor Necrosis Factor-alpha/therapeutic use ; Tumor Necrosis Factor Inhibitors/therapeutic use ; Cytokines
    Chemical Substances Tumor Necrosis Factor-alpha ; Tumor Necrosis Factor Inhibitors ; Cytokines
    Language English
    Publishing date 2023-07-05
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2162-4968
    ISSN (online) 2162-4968
    DOI 10.1007/s13679-023-00519-y
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  7. Article ; Online: Osteoprotegerin/Receptor Activator of Nuclear Factor-Kappa B Ligand/Receptor Activator of Nuclear Factor-Kappa B Axis in Obesity, Type 2 Diabetes Mellitus, and Nonalcoholic Fatty Liver Disease.

    Vachliotis, Ilias D / Polyzos, Stergios A

    Current obesity reports

    2023  Volume 12, Issue 2, Page(s) 147–162

    Abstract: Purpose of review: To summarize evidence on the potential involvement of the osteoprotegerin (OPG)/receptor activator of nuclear factor-kappa B (NF-κΒ) ligand (RANKL)/receptor activator of NF-κΒ (RANK) axis in the pathogenesis of metabolic diseases.: ... ...

    Abstract Purpose of review: To summarize evidence on the potential involvement of the osteoprotegerin (OPG)/receptor activator of nuclear factor-kappa B (NF-κΒ) ligand (RANKL)/receptor activator of NF-κΒ (RANK) axis in the pathogenesis of metabolic diseases.
    Recent findings: The OPG-RANKL-RANK axis, which has been originally involved in bone remodeling and osteoporosis, is now recognized as a potential contributor in the pathogenesis of obesity and its associated comorbidities, i.e., type 2 diabetes mellitus and nonalcoholic fatty liver disease. Besides bone, OPG and RANKL are also produced in adipose tissue and may be involved in the inflammatory process associated with obesity. Metabolically healthy obesity has been associated with lower circulating OPG concentrations, possibly representing a counteracting mechanism, while elevated serum OPG levels may reflect an increased risk of metabolic dysfunction or cardiovascular disease. OPG and RANKL have been also proposed as potential regulators of glucose metabolism and are potentially involved in the pathogenesis of type 2 diabetes mellitus. In clinical terms, type 2 diabetes mellitus has been consistently associated with increased serum OPG concentrations. With regard to nonalcoholic fatty liver disease, experimental data suggest a potential contribution of OPG and RANKL in hepatic steatosis, inflammation, and fibrosis; however, most clinical studies showed reduction in serum concentrations of OPG and RANKL. The emerging contribution of the OPG-RANKL-RANK axis to the pathogenesis of obesity and its associated comorbidities warrants further investigation by mechanistic studies and may have potential diagnostic and therapeutic implications.
    MeSH term(s) Humans ; Receptor Activator of Nuclear Factor-kappa B/metabolism ; Osteoprotegerin/metabolism ; Diabetes Mellitus, Type 2 ; Non-alcoholic Fatty Liver Disease ; NF-kappa B ; RANK Ligand/metabolism ; Ligands ; Obesity
    Chemical Substances Receptor Activator of Nuclear Factor-kappa B ; Osteoprotegerin ; NF-kappa B ; RANK Ligand ; Ligands
    Language English
    Publishing date 2023-05-19
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2162-4968
    ISSN (online) 2162-4968
    DOI 10.1007/s13679-023-00505-4
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  8. Article ; Online: Peptide Polyagonists for the Treatment of Nonalcoholic Fatty Liver Disease.

    Polyzos, Stergios A / Frühbeck, Gema / Kiortsis, Dimitrios N

    Current pharmaceutical design

    2024  Volume 29, Issue 41, Page(s) 3263–3265

    MeSH term(s) Humans ; Non-alcoholic Fatty Liver Disease/drug therapy ; Glucagon-Like Peptide 1 ; Insulin ; Peptides/pharmacology ; Peptides/therapeutic use ; Diabetes Mellitus, Type 2 ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents
    Chemical Substances Glucagon-Like Peptide 1 (89750-14-1) ; Insulin ; Peptides ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents
    Language English
    Publishing date 2024-01-10
    Publishing country United Arab Emirates
    Document type Editorial
    ZDB-ID 1304236-1
    ISSN 1873-4286 ; 1381-6128
    ISSN (online) 1873-4286
    ISSN 1381-6128
    DOI 10.2174/0113816128279822231211101522
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    Zs.A 4714: Show issues Location:
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  9. Article ; Online: Circulating leptin in patients with nonalcoholic fatty liver disease-related liver fibrosis: a systematic review and a meta-analysis.

    Makri, Evangelia S / Evripidou, Kleo / Polyzos, Stergios A

    Journal of gastroenterology and hepatology

    2024  Volume 39, Issue 5, Page(s) 806–817

    Abstract: Background and aim: Clinical data on the association between leptin levels and nonalcoholic fatty liver disease (NAFLD)-related liver fibrosis are conflicting. This meta-analysis aimed to compare circulating leptin between NAFLD patients with versus ... ...

    Abstract Background and aim: Clinical data on the association between leptin levels and nonalcoholic fatty liver disease (NAFLD)-related liver fibrosis are conflicting. This meta-analysis aimed to compare circulating leptin between NAFLD patients with versus without liver fibrosis or non-NAFLD controls.
    Methods: A systematic search was conducted in PubMed, Scopus, and the Cochrane Library. Fifteen studies were included, reporting data from 964 individuals (422 NAFLD patients with fibrosis, 297 NAFLD patients without fibrosis, 245 no-NAFLD controls).
    Results: Leptin standardized mean difference (SMD) was higher in NAFLD patients with fibrosis (F1-F4) than in controls (SMD: 2.27; 95% confidence interval [CI]: 0.81-3.73); however, this association did not remain robust after the exclusion of studies with morbidly obese individuals. No difference was observed in leptin SMD between NAFLD patients with fibrosis and those without fibrosis (F0), and NAFLD patients without fibrosis versus controls. Heterogeneity was high (I
    Conclusion: Circulating leptin was higher in NAFLD patients with liver fibrosis than non-NAFLD controls, an association, however, attenuated after the exclusion of a study with morbidly obese individuals. Circulating leptin was not different between NAFLD patients with and without fibrosis, or NAFLD patients without fibrosis and controls.
    MeSH term(s) Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/complications ; Leptin/blood ; Humans ; Liver Cirrhosis/blood ; Liver Cirrhosis/etiology ; Insulin Resistance ; Biomarkers/blood ; Male ; Female
    Chemical Substances Leptin ; Biomarkers
    Language English
    Publishing date 2024-01-18
    Publishing country Australia
    Document type Journal Article ; Systematic Review ; Meta-Analysis
    ZDB-ID 632882-9
    ISSN 1440-1746 ; 0815-9319
    ISSN (online) 1440-1746
    ISSN 0815-9319
    DOI 10.1111/jgh.16480
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    Zs.MO 299: Show issues

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  10. Article ; Online: Metreleptin for the treatment of lipodystrophy: leading the way among novel therapeutics for this unmet clinical need.

    Polyzos, Stergios A / Mantzoros, Christos S

    Current medical research and opinion

    2022  Volume 38, Issue 6, Page(s) 885–888

    MeSH term(s) Humans ; Leptin/analogs & derivatives ; Leptin/therapeutic use ; Lipodystrophy/drug therapy
    Chemical Substances Leptin ; metreleptin (TL60C27RLH)
    Language English
    Publishing date 2022-04-12
    Publishing country England
    Document type Editorial
    ZDB-ID 80296-7
    ISSN 1473-4877 ; 0300-7995
    ISSN (online) 1473-4877
    ISSN 0300-7995
    DOI 10.1080/03007995.2022.2059974
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