abscisic-acid and Glucose-Intolerance

abscisic-acid has been researched along with Glucose-Intolerance* in 2 studies

Other Studies

2 other study(ies) available for abscisic-acid and Glucose-Intolerance

ArticleYear
Abscisic Acid Treatment in Patients with Prediabetes.
    Nutrients, 2020, Sep-24, Volume: 12, Issue:10

    to evaluate the effects of abscisic acid (ABA), contained in dwarf peaches, on the regression of impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) conditions.. sixty-five patients with IFG or IGT were randomized to take ABA or placebo for 3 months. We evaluated: fasting plasma glucose (FPG), postprandial plasma glucose (PPG), glycated hemoglobin (HbA. a significant reduction of HbA. abscisic acid can be effective in ameliorating glyco-metabolic compensation and in reducing inflammatory status in patients with IFG or IGT.

    Topics: Abscisic Acid; Aged; Alanine Transaminase; Aspartate Aminotransferases; Blood Glucose; C-Reactive Protein; Cholesterol, HDL; Cholesterol, LDL; Dietary Supplements; Double-Blind Method; Fasting; Female; Glucose Clamp Technique; Glucose Intolerance; Glucose Tolerance Test; Glycated Hemoglobin; Humans; Insulin; Insulin Resistance; Male; Middle Aged; Postprandial Period; Prediabetic State; Randomized Controlled Trials as Topic

2020
Abscisic acid synergizes with rosiglitazone to improve glucose tolerance and down-modulate macrophage accumulation in adipose tissue: possible action of the cAMP/PKA/PPAR γ axis.
    Clinical nutrition (Edinburgh, Scotland), 2010, Volume: 29, Issue:5

    Abscisic acid (ABA) is effective in preventing insulin resistance and obesity-related inflammation through a PPAR γ-dependent mechanism. The objective of this study was to assess the efficacy ABA in improving glucose homeostasis and suppress inflammation when administered in combination with rosiglitazone (Ros) and to determine whether PPAR γ activation by ABA is initiated via cAMP/protein kinase A (PKA) signaling.. Obese db/db mice were fed high-fat diets containing 0, 10, or 70 mg/kg Ros with and without racemic ABA (100 mg/kg) for 60 days. Glucose tolerance and fasting insulin levels were assessed at 6 and 8 weeks, respectively, and adipose tissue macrophage (ATM) infiltration was examined by flow cytometry. Gene expression was examined on white adipose tissue (WAT) and stromal vascular cells (SVCs) cultured with ABA, Ros, or an ABA/Ros combination.. Both Ros and ABA improved glucose tolerance, and ABA decreased plasma insulin levels while having no effect on Ros-induced weight gain. ABA in combination with low-dose Ros (10 mg/kg; Roslo) synergistically inhibited ATM infiltration. Treatment of SVCs with Ros, ABA or ABA/Ros suppressed expression of the M1 marker CCL17. ABA and Ros synergistically increased PPAR γ activity and pretreatment with a cAMP-inhibitor or a PKA-inhibitor abrogated ABA-induced PPAR γ activation.. ABA and Ros act synergistically to modulate PPAR γ activity and macrophage accumulation in WAT and ABA enhances PPAR γ activity through a membrane-initiated mechanism dependent on cAMP/PKA signaling.

    Topics: Abscisic Acid; Adipose Tissue; Animals; Blood Glucose; Cyclic AMP-Dependent Protein Kinases; Data Collection; Diabetes Mellitus; Glucose Intolerance; Inflammation; Insulin; Macrophages; Mice; Mice, Obese; Obesity; PPAR gamma; Rosiglitazone; Thiazolidinediones

2010