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  1. Article ; Online: Measuring and estimating insulin resistance in clinical and research settings.

    Gastaldelli, Amalia

    Obesity (Silver Spring, Md.)

    2022  Volume 30, Issue 8, Page(s) 1549–1563

    Abstract: The article discusses how to measure insulin resistance in muscle, liver, and adipose tissue in human participants. The most frequently used methodologies to evaluate insulin resistance are described in detail starting from the gold standard, that is, ... ...

    Abstract The article discusses how to measure insulin resistance in muscle, liver, and adipose tissue in human participants. The most frequently used methodologies to evaluate insulin resistance are described in detail starting from the gold standard, that is, the euglycemic hyperinsulinemic clamp, to the intravenous glucose tolerance test, surrogate indices based on fasting measurements, or dynamic tests (such as oral glucose or mixed meal tolerance tests). The accuracy, precision, and reproducibility of the tests as well as cutoff values are reported.
    MeSH term(s) Blood Glucose ; Glucose Clamp Technique ; Glucose Intolerance ; Glucose Tolerance Test ; Humans ; Insulin ; Insulin Resistance/physiology ; Reproducibility of Results
    Chemical Substances Blood Glucose ; Insulin
    Language English
    Publishing date 2022-08-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2230457-5
    ISSN 1930-739X ; 1071-7323 ; 1930-7381
    ISSN (online) 1930-739X
    ISSN 1071-7323 ; 1930-7381
    DOI 10.1002/oby.23503
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4061: Show issues Location:
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  2. Article: Is it necessary to target lipid metabolism in different organs for effective treatment of NASH?-the results of the Pan-PPAR Lanifibranor trial.

    Gastaldelli, Amalia

    Hepatobiliary surgery and nutrition

    2021  Volume 11, Issue 3, Page(s) 481–484

    Language English
    Publishing date 2021-01-29
    Publishing country China (Republic : 1949- )
    Document type Editorial ; Comment
    ZDB-ID 2812398-0
    ISSN 2304-389X ; 2304-3881
    ISSN (online) 2304-389X
    ISSN 2304-3881
    DOI 10.21037/hbsn-21-569
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Hepatic glucose metabolism in the steatotic liver.

    Scoditti, Egeria / Sabatini, Silvia / Carli, Fabrizia / Gastaldelli, Amalia

    Nature reviews. Gastroenterology & hepatology

    2024  

    Abstract: The liver is central in regulating glucose homeostasis, being the major contributor to endogenous glucose production and the greatest reserve of glucose as glycogen. It is both a target and regulator of the action of glucoregulatory hormones. Hepatic ... ...

    Abstract The liver is central in regulating glucose homeostasis, being the major contributor to endogenous glucose production and the greatest reserve of glucose as glycogen. It is both a target and regulator of the action of glucoregulatory hormones. Hepatic metabolic functions are altered in and contribute to the highly prevalent steatotic liver disease (SLD), including metabolic dysfunction-associated SLD (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH). In this Review, we describe the dysregulation of hepatic glucose metabolism in MASLD and MASH and associated metabolic comorbidities, and how advances in techniques and models for the assessment of hepatic glucose fluxes in vivo have led to the identification of the mechanisms related to the alterations in glucose metabolism in MASLD and comorbidities. These fluxes can ultimately increase hepatic glucose production concomitantly with fat accumulation and alterations in the secretion and action of glucoregulatory hormones. No pharmacological treatment has yet been approved for MASLD or MASH, but some antihyperglycaemic drugs approved for treating type 2 diabetes have shown positive effects on hepatic glucose metabolism and hepatosteatosis. A deep understanding of how MASLD affects glucose metabolic fluxes and glucoregulatory hormones might assist in the early identification of at-risk individuals and the use or development of targeted therapies.
    Language English
    Publishing date 2024-02-02
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2493722-8
    ISSN 1759-5053 ; 1759-5045
    ISSN (online) 1759-5053
    ISSN 1759-5045
    DOI 10.1038/s41575-023-00888-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Editorial: Mechanisms for the Alteration in the Crosstalk Among Insulin-Sensitive Tissues.

    Schiavon, Michele / Gastaldelli, Amalia

    Frontiers in endocrinology

    2022  Volume 13, Page(s) 883659

    MeSH term(s) Cell Physiological Phenomena ; Humans ; Insulin ; Insulin Resistance
    Chemical Substances Insulin
    Language English
    Publishing date 2022-04-14
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2022.883659
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  5. Article ; Online: Hunting for Progressive NAFLD in Type 2 Diabetes: Do Not Trust Liver Enzymes!

    Scoditti, Egeria / Marchesini, Giulio / Gastaldelli, Amalia

    Diabetes care

    2023  Volume 46, Issue 7, Page(s) 1332–1334

    MeSH term(s) Humans ; Biopsy ; Diabetes Mellitus, Type 2/epidemiology ; Fibrosis ; Liver/pathology ; Non-alcoholic Fatty Liver Disease/epidemiology ; Outpatients ; Prevalence ; Prospective Studies
    Language English
    Publishing date 2023-06-20
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 441231-x
    ISSN 1935-5548 ; 0149-5992
    ISSN (online) 1935-5548
    ISSN 0149-5992
    DOI 10.2337/dci23-0027
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    Zs.MO 365: Show issues

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  6. Article ; Online: Role of Insulin Clearance in Insulin Action and Metabolic Diseases.

    Ghadieh, Hilda E / Gastaldelli, Amalia / Najjar, Sonia M

    International journal of molecular sciences

    2023  Volume 24, Issue 8

    Abstract: The year 2021 marked the centenary of the discovery of insulin [ ... ]. ...

    Abstract The year 2021 marked the centenary of the discovery of insulin [...].
    MeSH term(s) Humans ; Insulin/metabolism ; Insulin Resistance ; Insulin, Regular, Human ; Metabolic Diseases
    Chemical Substances Insulin ; Insulin, Regular, Human
    Language English
    Publishing date 2023-04-12
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24087156
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  7. Article: Obesity-Related Insulin Resistance: The Central Role of Adipose Tissue Dysfunction.

    Mocciaro, Gabriele / Gastaldelli, Amalia

    Handbook of experimental pharmacology

    2022  Volume 274, Page(s) 145–164

    Abstract: Obesity is a key player in the onset and progression of insulin resistance (IR), a state by which insulin-sensitive cells fail to adequately respond to insulin action. IR is a reversible condition, but if untreated leads to type 2 diabetes alongside ... ...

    Abstract Obesity is a key player in the onset and progression of insulin resistance (IR), a state by which insulin-sensitive cells fail to adequately respond to insulin action. IR is a reversible condition, but if untreated leads to type 2 diabetes alongside increasing cardiovascular risk. The link between obesity and IR has been widely investigated; however, some aspects are still not fully characterized.In this chapter, we introduce key aspects of the pathophysiology of IR and its intimate connection with obesity. Specifically, we focus on the role of adipose tissue dysfunction (quantity, quality, and distribution) as a driver of whole-body IR. Furthermore, we discuss the obesity-related lipidomic remodeling occurring in adipose tissue, liver, and skeletal muscle. Key mechanisms linking lipotoxicity to IR in different tissues and metabolic alterations (i.e., fatty liver and diabetes) and the effect of weight loss on IR are also reported while highlighting knowledge gaps.
    MeSH term(s) Adipose Tissue/metabolism ; Diabetes Mellitus, Type 2/etiology ; Humans ; Insulin Resistance/physiology ; Insulins/metabolism ; Obesity/metabolism
    Chemical Substances Insulins
    Language English
    Publishing date 2022-02-21
    Publishing country Germany
    Document type Journal Article
    ISSN 0171-2004
    ISSN 0171-2004
    DOI 10.1007/164_2021_573
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    Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
     danach: Sign. bei den Einzelbänden: Show issues

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  8. Article ; Online: Insulin resistance and reduced metabolic flexibility: cause or consequence of NAFLD?

    Gastaldelli, Amalia

    Clinical science (London, England : 1979)

    2017  Volume 131, Issue 22, Page(s) 2701–2704

    Abstract: Whether non-alcoholic fatty liver disease (NAFLD) precedes insulin resistance (IR) or IR preludes/causes NAFLD has been long debated. Recent studies have shown that there are two phenotypes of NAFLD, 'genetic' vs 'metabolic' NAFLD. The former patients ... ...

    Abstract Whether non-alcoholic fatty liver disease (NAFLD) precedes insulin resistance (IR) or IR preludes/causes NAFLD has been long debated. Recent studies have shown that there are two phenotypes of NAFLD, 'genetic' vs 'metabolic' NAFLD. The former patients are more at risk of hepatocellular carcinoma and chronic liver disease the latter are more IR and at increased risk of type 2 diabetes (T2D). Even if they are not yet diabetics, from a metabolic point of view having NAFLD is equivalent to T2D with reduced peripheral glucose disposal and impaired suppression of hepatic glucose production, but without fasting hyperglycaemia. T2D develops only when hepatic autoregulation is lost and glucose production exceeds the capacity of muscle glucose disposal.In NAFLD adipocytes are resistant to the effect of insulin, lipolysis is increased and excess plasma free fatty acids (FFA) are taken up by other organs (mainly liver) where they are stored as lipid droplets or oxidized. Increased adiposity is associated with worsen severity of both 'genetic' and 'metabolic' NAFLD. FFA oxidative metabolism is increased in NAFLD and not shifted towards glucose during insulin infusion. Although this reduced metabolic flexibility is an early predictor of T2D, it can be seen also as a protective mechanism against excess FFA.In conclusion, IR precedes and causes 'metabolic' NAFLD, but not 'genetic' NAFLD. Reduced metabolic flexibility in NAFLD might be seen as a protective mechanism against FFA overflow, but together with IR remains a strong risk factor for T2D that develops with the worsening of hepatic regulation of glucose production.
    MeSH term(s) Adipose Tissue/metabolism ; Animals ; Biomarkers/blood ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/diagnosis ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/genetics ; Energy Metabolism/genetics ; Genetic Predisposition to Disease ; Humans ; Insulin/blood ; Insulin Resistance/genetics ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/genetics ; Obesity/blood ; Obesity/diagnosis ; Obesity/epidemiology ; Obesity/genetics ; Phenotype ; Prognosis ; Risk Factors ; Signal Transduction
    Chemical Substances Biomarkers ; Blood Glucose ; Insulin
    Language English
    Publishing date 2017-11-15
    Publishing country England
    Document type Editorial
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20170987
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    Ua VI Zs.220: Show issues Location:
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  9. Article ; Online: Disparity-filtered differential correlation network analysis: a case study on CRC metabolomics.

    Sabatini, Silvia / Gastaldelli, Amalia

    Journal of integrative bioinformatics

    2021  Volume 18, Issue 4

    Abstract: Differential network analysis has become a widely used technique to investigate changes of interactions among different conditions. Although the relationship between observed interactions and biochemical mechanisms is hard to establish, differential ... ...

    Abstract Differential network analysis has become a widely used technique to investigate changes of interactions among different conditions. Although the relationship between observed interactions and biochemical mechanisms is hard to establish, differential network analysis can provide useful insights about dysregulated pathways and candidate biomarkers. The available methods to detect differential interactions are heterogeneous and often rely on assumptions that are unrealistic in many applications. To address these issues, we develop a novel method for differential network analysis, using the so-called disparity filter as network reduction technique. In addition, we propose a classification model based on the inferred network interactions. The main novelty of this work lies in its ability to preserve connections that are statistically significant with respect to a null model without favouring any resolution scale, as a hard threshold would do, and without Gaussian assumptions. The method was tested using a published metabolomic dataset on colorectal cancer (CRC). Detected hub metabolites were consistent with recent literature and the classifier was able to distinguish CRC from polyp and healthy subjects with great accuracy. In conclusion, the proposed method provides a new simple and effective framework for the identification of differential interaction patterns and improves the biological interpretation of metabolomics data.
    MeSH term(s) Biomarkers ; Colorectal Neoplasms/diagnosis ; Humans ; Metabolomics
    Chemical Substances Biomarkers
    Language English
    Publishing date 2021-11-19
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2147212-9
    ISSN 1613-4516 ; 1432-4385
    ISSN (online) 1613-4516
    ISSN 1432-4385
    DOI 10.1515/jib-2021-0030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Differential effect of endogenous glucagon-like peptide-1 on prandial glucose counterregulatory response to hypoglycaemia in humans with and without bariatric surgery.

    Honka, Henri / Gastaldelli, Amalia / Pezzica, Samantha / Peterson, Richard / DeFronzo, Ralph / Salehi, Marzieh

    Diabetes, obesity & metabolism

    2024  

    Abstract: Aim: To determine the effect of endogenous glucagon-like peptide 1 (GLP-1) on prandial counterregulatory response to hypoglycaemia after gastric bypass (GB).: Materials and methods: Glucose fluxes, and islet-cell and gut hormone responses before and ... ...

    Abstract Aim: To determine the effect of endogenous glucagon-like peptide 1 (GLP-1) on prandial counterregulatory response to hypoglycaemia after gastric bypass (GB).
    Materials and methods: Glucose fluxes, and islet-cell and gut hormone responses before and after mixed-meal ingestion, were compared during a hyperinsulinaemic-hypoglycaemic (~3.2 mmol/L) clamp with and without a GLP-1 receptor (GLP-1R) antagonist exendin-(9-39) infusion in non-diabetic patients who had previously undergone GB compared to matched participants who had previously undergone sleeve gastrectomy (SG) and non-surgical controls.
    Results: Exendin-(9-39) infusion raised prandial endogenous glucose production (EGP) response to insulin-induced hypoglycaemia in the GB group but had no consistent effect on EGP response among the SG group or non-surgical controls (p < 0.05 for interaction). The rates of systemic appearance of ingested glucose or prandial glucose utilization did not differ among the three groups or between studies with and without exendin-(9-39) infusion. Blockade of GLP-1R had no effect on insulin secretion or insulin action but enhanced prandial glucagon in all three groups.
    Conclusions: These results indicate that impaired post-meal glucose counterregulatory response to hypoglycaemia after GB is partly mediated by endogenous GLP-1, highlighting a novel pathogenic mechanism of GLP-1 in developing hypoglycaemia in this population.
    Language English
    Publishing date 2024-04-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 1454944-x
    ISSN 1463-1326 ; 1462-8902
    ISSN (online) 1463-1326
    ISSN 1462-8902
    DOI 10.1111/dom.15570
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    Zs.A 5442: Show issues Location:
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