abscisic-acid and Diabetes-Mellitus

Abscisic acid (ABA), long known as a plant stress hormone, is present and functionally active in organisms other than those pertaining to the land plant kingdom, including cyanobacteria, fungi, algae, protozoan parasites, lower Metazoa, and mammals. The ancient, cross-kingdom role of this stress hormone allows ABA and its signaling pathway to control cell responses to environmental stimuli in diverse organisms such as marine sponges, higher plants, and humans. Recent advances in our knowledge about the physiological role of ABA and of its mammalian receptors in the control of energy metabolism and mitochondrial function in myocytes, adipocytes, and neuronal cells allow us to foresee therapeutic applications for ABA in the fields of pre-diabetes, diabetes, and cardio- and neuro-protection. Vegetal extracts titrated in their ABA content have shown both efficacy and tolerability in preliminary clinical studies. As the prevalence of glucose intolerance, diabetes, and cardiovascular and neurodegenerative diseases is steadily increasing in both industrialized and rapidly developing countries, new and cost-efficient therapeutics to combat these ailments are much needed to ensure disease-free aging for the current and future working generations.

Topics: Abscisic Acid; Animals; Diabetes Mellitus; Embryophyta; Hormones; Humans; Mammals; Myocytes, Cardiac; Neuroprotection; Plant Growth Regulators

Topics: 11-beta-Hydroxysteroid Dehydrogenase Type 1; Abelmoschus; Abscisic Acid; Aldehyde Reductase; Computer Simulation; Diabetes Mellitus; Enzyme Inhibitors; Glucokinase; Glutamine; Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing); Glycogen Synthase Kinase 3; Humans; Hypoglycemic Agents; Molecular Docking Simulation; PPAR gamma; Proteins; Sirtuins

Abscisic acid (ABA) is a plant hormone active also in mammals where it regulates, at nanomolar concentrations, blood glucose homeostasis. Here we investigated the mechanism through which low-dose ABA controls glycemia and glucose fate. ABA stimulated uptake of the fluorescent glucose analog 2-NBDG by L6, and of [

Topics: 4-Chloro-7-nitrobenzofurazan; Abscisic Acid; AMP-Activated Protein Kinase Kinases; Animals; Cell Line; Deoxyglucose; Diabetes Mellitus; Disease Models, Animal; Glucose; Insulin; Male; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Skeletal; Myoblasts; Protein Kinases; Rats; Rats, Wistar; RNA, Small Interfering; TRPM Cation Channels

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Topics: Abelmoschus; Abscisic Acid; Chromatography, High Pressure Liquid; Diabetes Mellitus; Dietary Supplements; Hypoglycemic Agents; Malvaceae; Plant Extracts

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