TY - JOUR
T1 - In vitro and in vivo inhibition of intestinal glucose transport by guava (Psidium guajava) extracts
AU - Müller, Ulrike
AU - Stübl, Flora
AU - Schwarzinger, Bettina
AU - Sandner, Georg Philipp
AU - Iken, Marcus
AU - Himmelsbach, Markus
AU - Schwarzinger, Clemens
AU - Ollinger, Nicole
AU - Stadlbauer, Verena
AU - Höglinger, Otmar
AU - Lanzerstorfer, Peter
AU - Weghuber, Julian
PY - 2018/6
Y1 - 2018/6
N2 - Scope: Known pharmacological activities of guava (Psidium guajava) include modulation of blood glucose levels. However, mechanistic details remain unclear in many cases. Methods and results: This study investigated the effects of different guava leaf and fruit extracts on intestinal glucose transport in vitro and on postprandial glucose levels in vivo. Substantial dose- and time-dependent glucose transport inhibition (up to 80%) was observed for both guava fruit and leaf extracts, at conceivable physiological concentrations in Caco-2 cells. Using sodium-containing (both glucose transporters, sodium-dependent glucose transporter 1 [SGLT1] and glucose transporter 2 [GLUT2], are active) and sodium-free (only GLUT2 is active) conditions, we show that inhibition of GLUT2 was greater than that of SGLT1. Inhibitory properties of guava extracts also remained stable after digestive juice treatment, indicating a good chemical stability of the active substances. Furthermore, we could unequivocally show that guava extracts significantly reduced blood glucose levels (≈fourfold reduction) in a time-dependent manner in vivo (C57BL/6N mice). Extracts were characterized with respect to their main putative bioactive compounds (polyphenols) using HPLC and LC-MS. Conclusion: The data demonstrated that guava leaf and fruit extracts can potentially contribute to the regulation of blood glucose levels.
AB - Scope: Known pharmacological activities of guava (Psidium guajava) include modulation of blood glucose levels. However, mechanistic details remain unclear in many cases. Methods and results: This study investigated the effects of different guava leaf and fruit extracts on intestinal glucose transport in vitro and on postprandial glucose levels in vivo. Substantial dose- and time-dependent glucose transport inhibition (up to 80%) was observed for both guava fruit and leaf extracts, at conceivable physiological concentrations in Caco-2 cells. Using sodium-containing (both glucose transporters, sodium-dependent glucose transporter 1 [SGLT1] and glucose transporter 2 [GLUT2], are active) and sodium-free (only GLUT2 is active) conditions, we show that inhibition of GLUT2 was greater than that of SGLT1. Inhibitory properties of guava extracts also remained stable after digestive juice treatment, indicating a good chemical stability of the active substances. Furthermore, we could unequivocally show that guava extracts significantly reduced blood glucose levels (≈fourfold reduction) in a time-dependent manner in vivo (C57BL/6N mice). Extracts were characterized with respect to their main putative bioactive compounds (polyphenols) using HPLC and LC-MS. Conclusion: The data demonstrated that guava leaf and fruit extracts can potentially contribute to the regulation of blood glucose levels.
KW - GLUT2
KW - SGLT1
KW - guava extract
KW - intestinal glucose transport
KW - postprandial blood glucose
KW - Caco-2 Cells
KW - Sodium-Glucose Transporter 1/genetics
KW - Humans
KW - Mice, Inbred C57BL
KW - Biological Transport/drug effects
KW - Polyphenols/analysis
KW - Fruit/chemistry
KW - Glucose Transporter Type 5/genetics
KW - Intestinal Mucosa/drug effects
KW - Plant Extracts/analysis
KW - Animals
KW - Psidium/chemistry
KW - Plant Leaves/chemistry
KW - Postprandial Period
KW - Glucose Transporter Type 2/genetics
KW - Female
KW - Glucose/metabolism
KW - Hypoglycemic Agents/pharmacology
UR - http://www.scopus.com/inward/record.url?scp=85048636867&partnerID=8YFLogxK
U2 - 10.1002/mnfr.201701012
DO - 10.1002/mnfr.201701012
M3 - Article
C2 - 29688623
SN - 1613-4133
VL - 62
JO - Molecular nutrition and food research
JF - Molecular nutrition and food research
IS - 11
M1 - 1701012
ER -