Abstract
Abscisic acid (ABA) is a hormone with a very long evolutionary history, dating back to the earliest living organisms, of which modern (ABA-producing) cyanobacteria are likely the descendants, well before separation of the plant and animal kingdoms, with a conserved role as a signal regulating cell responses to environmental challenges. In mammals, nanomolar ABA controls the metabolic response to glucose availability by stimulating glucose uptake in skeletal muscle and adipose tissue with an insulin-independent mechanism and increasing energy expenditure in the brown and white adipose tissues. Activation by ABA of AMP-dependent kinase (AMPK), in contrast to the insulin-induced activation of AMPK-inhibiting Akt, is responsible for stimulation of GLUT4-mediated muscle glucose uptake, and for the browning effect on white adipocytes. Intake of micrograms per Kg body weight of ABA improves glucose tolerance in both normal and in borderline subjects and chronic intake of such a dose of ABA improves blood glucose, lipids and morphometric parameters (waist circumference and body mass index) in borderline subjects for prediabetes and the metabolic syndrome. This review summarizes the most recent results obtained in vivo with microgram amounts of ABA, the role of the receptor LANCL2 in the hormone’s action and the significance of the endowment by mammals of two different hormones controlling the metabolic response to glucose availability. Finally, open issues in need of further investigation and perspectives for the clinical use of nutraceutical ABA are discussed.
Highlights
In the same study, the authors showed that nanomolar Abscisic acid (ABA) stimulated glucose uptake, quantitatively to insulin, in rat L6 myoblasts and in murine 3T3-L1 cells differentiated to adipocytes, by increasing GLUT-4 translocation to the plasma membrane
We focused our attention on the metabolic function of the ABA/LANCL2 system on glycemic and lipidemic control, neglecting other important aspects of ABA physiology in mammals, such as its regulatory role in inflammation, for which we redirect the reader to the excellent review by Lievens et al [44]
Studies on murine model(s) of insulin-dependent diabetes could provide preclinical evidence supporting the use of oral low-dose ABA to improve glycemia control in combination with insulin
Summary
2-cis, 4-trans-Abscisic acid (ABA) is a 15-carbon weak acid (pKa 4.8) terpenoid hormone (Figure 1). These functional responses were mediated by a signaling pathway challenges Starting from therange observation that cADPR waseffects involved in the Ca2+ signaling leadingcells: to insulin release, concentration has pro-inflammatory on mammalian innate immune a conserved the effect ofpathway. Micromolar insulin signaling the activation the ADP-ribosyl cyclase CD38 andstimulated the production of release vitro, from rat insulinoma cells and from isolated islets [12], and vivo, inwas the the Cain2+-mobilizing second messenger cADPR.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
