Abstract
The plant hormone abscisic acid (ABA) is present and active in humans, regulating glucose homeostasis. In normal glucose tolerant (NGT) human subjects, plasma ABA (ABAp) increases 5-fold after an oral glucose load. The aim of this study was to assess the effect of an oral glucose load on ABAp in type 2 diabetes (T2D) subjects. We chose two sub-groups of patients who underwent an oral glucose load for diagnostic purposes: i) 9 treatment-naive T2D subjects, and ii) 9 pregnant women with gestational diabetes (GDM), who underwent the glucose load before and 8–12 weeks after childbirth. Each group was compared with matched NGT controls. The increase of ABAp in response to glucose was found to be abrogated in T2D patients compared to NGT controls. A similar result was observed in the women with GDM compared to pregnant NGT controls; 8–12 weeks after childbirth, however, fasting ABAp and ABAp response to glucose were restored to normal in the GDM subjects, along with glucose tolerance. We also retrospectively compared fasting ABAp before and after bilio-pancreatic diversion (BPD) in obese, but not diabetic subjects, and in obese T2D patients, in which BPD resulted in the resolution of diabetes. Compared to pre-BPD values, basal ABAp significantly increased 1 month after BPD in T2D as well as in NGT subjects, in parallel with a reduction of fasting plasma glucose. These results indicate an impaired hyperglycemia-induced ABAp increase in T2D and in GDM and suggest a beneficial effect of elevated ABAp on glycemic control.
Highlights
The phytohormone abscisic acid (ABA) lies at the interface between abiotic stress and metabolic signaling in plants, regulating vital functions [1]
To determine whether the ABA response to oral glucose was modified in type 2 diabetes (T2D), plasma samples from 11 patients with impaired fasting glycemia, who underwent an oral glucose tolerance test (OGTT) for diagnostic purposes, were collected immediately before and 15, 30, 60, 90, and 120 minutes after intake of glucose; in 9 out of these 11 subjects, T2D was confirmed by the test
As a result of the failure of ABAp to increase in the T2D patients, the AUC of ABAp during the OGTT was significantly lower in these subjects compared to normal glucose tolerant (NGT) controls (Table 1)
Summary
The phytohormone abscisic acid (ABA) lies at the interface between abiotic stress and metabolic signaling in plants, regulating vital functions [1]. ABA was found to play a conserved role as a “stress hormone” in lower Metazoa, regulating animal responses to temperature and light [2, 3], and in mammals, regulating the activation of innate immune cells [4, 5] and glucose homeostasis [6,7,8]. Mammalian pancreatic β-cells release ABA in response to glucose and ABA in turn potentiates glucose-dependent and stimulates glucose-independent insulin secretion, suggesting the existence of an autocrine/paracrine feed-forward loop [6]. Glucagon-like peptide 1 (GLP-1) enhances ABA secretion from glucose-stimulated pancreatic β-cells in vitro [7]. ABA role in glucose homeostasis prompts the hypothesis that diabetes mellitus is associated with an impaired ABA response. In the db/db mouse model of obesity-induced type 2 diabetes (T2D), supplementation of a high-fat diet with ABA results in improved glucose tolerance [8]
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