Phytochemical and in vitro antioxidant assessment of Yoyo bitters

In this paper, herbal bitters are widely used due to their numerous acclaimed health benefits in many Nigerian homes; however, many have not been subjected to scientific scrutiny. The aim of this study was to determine the phytochemical composition and antioxidant capacity of a non-alcoholic polyherbal formulation, Yoyo bitters, towards validating its broad pharmacological claims. The phytochemical components of Yoyo bitters were ascertained by phytochemical screening assays and gas chromatography-mass spectrometry (GC-MS). The antioxidant activity was investigated in vitro using 2,2-diphenyl-1-picryhydrazyl (DPPH) radical, hydrogen peroxide (H2O2) scavenging activity, total antioxidant capacity (TAC) and ferric reducing antioxidant power (FRAP) assays. Qualitative phytochemical analysis of Yoyo bitters showed the presence of saponins, tannins, flavonoids, terpenoids, cardiac glycosides and anthocyanins. The total phenols, flavonoids, flavanols, tannins and carotenoids content were 14.741 ±0.64 mg GAE/ml, 0.152 ±0.01 mg RE/ml, 0.437 ±0.02 mg RE/ml, 0.368 ±0.04 mg TAE/ml and 0.016 ±0.00 mg CAE/ml respectively. GC-MS chromatogram revealed the presence of forty-three (43) phytochemical compounds with D-allose (41.81%), 1,6-anhydro-beta-D-glucofuranose (24.15%), 5-hydroxymethylfurfural (8.02%) and Z-6-pentadecen-1-ol acetate (3.50%) as the most abundant constituents. Yoyo bitters demonstrated effective antioxidant activity against DPPH and H2O2 with IC50 values of 0.492 mg/ml and 0.629 mg/ml respectively compared to ascorbic acid of 0.161 mg/ml and 0.130 mg/ml respectively. Total antioxidant capacity and ferric reducing antioxidant power of Yoyo bitters were 0.432 mg AAE/ml and 2.236 mg AAE/ml respectively. This study validates the antioxidant capacity of Yoyo bitters and provides chemical basis for its acclaimed pharmacological actions

Stimulating intestinal GIP release reduces food intake and body weight in mice.

OBJECTIVE: Glucose dependent insulinotropic polypeptide (GIP) is well established as an incretin hormone, boosting glucose-dependent insulin secretion. However, whilst anorectic actions of its sister-incretin glucagon-like peptide-1 (GLP-1) are well established, a physiological role for GIP in appetite regulation is controversial, despite the superior weight loss seen in preclinical models and humans with GLP-1/GIP dual receptor agonists compared with GLP-1R agonism alone. METHODS: We generated a mouse model in which GIP expressing K-cells can be activated through hM3Dq Designer Receptor Activated by Designer Drugs (DREADD, GIP-Dq) to explore physiological actions of intestinally-released GIP. RESULTS: In lean mice, Dq-stimulation of GIP expressing cells increased plasma GIP to levels similar to those found postprandially. The increase in GIP was associated with improved glucose tolerance, as expected, but also triggered an unexpected robust inhibition of food intake. Validating that this represented a response to intestinally-released GIP, the suppression of food intake was prevented by injecting mice peripherally or centrally with antagonistic GIPR-antibodies, and was reproduced in an intersectional model utilising Gip-Cre/Villin-Flp to limit Dq transgene expression to K-cells in the intestinal epithelium. The effects of GIP cell activation were maintained in diet induced obese mice, in which chronic K-cell activation reduced food intake and attenuated body weight gain. CONCLUSIONS: These studies establish a physiological gut-brain GIP-axis regulating food intake in mice, adding to the multi-faceted metabolic effects of GIP which need to be taken into account when developing GIPR-targeted therapies for obesity and diabetes