Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans
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Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. / Kuhre, Rune Ehrenreich; Gribble, Fiona M; Hartmann, Bolette; Reimann, Frank; Windeløv, Johanne A; Rehfeld, Jens F; Holst, Jens Juul.
In: American Journal of Physiology: Gastrointestinal and Liver Physiology, Vol. 306, No. 7, 01.04.2014, p. G622-30.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans
AU - Kuhre, Rune Ehrenreich
AU - Gribble, Fiona M
AU - Hartmann, Bolette
AU - Reimann, Frank
AU - Windeløv, Johanne A
AU - Rehfeld, Jens F
AU - Holst, Jens Juul
PY - 2014/4/1
Y1 - 2014/4/1
N2 - Nutrients often stimulate gut hormone secretion, but the effects of fructose are incompletely understood. We studied the effects of fructose on a number of gut hormones with particular focus on glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). In healthy humans, fructose intake caused a rise in blood glucose and plasma insulin and GLP-1, albeit to a lower degree than isocaloric glucose. Cholecystokinin secretion was stimulated similarly by both carbohydrates, but neither peptide YY3-36 nor glucagon secretion was affected by either treatment. Remarkably, while glucose potently stimulated GIP release, fructose was without effect. Similar patterns were found in the mouse and rat, with both fructose and glucose stimulating GLP-1 secretion, whereas only glucose caused GIP secretion. In GLUTag cells, a murine cell line used as model for L cells, fructose was metabolized and stimulated GLP-1 secretion dose-dependently (EC50 = 0.155 mM) by ATP-sensitive potassium channel closure and cell depolarization. Because fructose elicits GLP-1 secretion without simultaneous release of glucagonotropic GIP, the pathways underlying fructose-stimulated GLP-1 release might be useful targets for type 2 diabetes mellitus and obesity drug development.
AB - Nutrients often stimulate gut hormone secretion, but the effects of fructose are incompletely understood. We studied the effects of fructose on a number of gut hormones with particular focus on glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). In healthy humans, fructose intake caused a rise in blood glucose and plasma insulin and GLP-1, albeit to a lower degree than isocaloric glucose. Cholecystokinin secretion was stimulated similarly by both carbohydrates, but neither peptide YY3-36 nor glucagon secretion was affected by either treatment. Remarkably, while glucose potently stimulated GIP release, fructose was without effect. Similar patterns were found in the mouse and rat, with both fructose and glucose stimulating GLP-1 secretion, whereas only glucose caused GIP secretion. In GLUTag cells, a murine cell line used as model for L cells, fructose was metabolized and stimulated GLP-1 secretion dose-dependently (EC50 = 0.155 mM) by ATP-sensitive potassium channel closure and cell depolarization. Because fructose elicits GLP-1 secretion without simultaneous release of glucagonotropic GIP, the pathways underlying fructose-stimulated GLP-1 release might be useful targets for type 2 diabetes mellitus and obesity drug development.
KW - Administration, Oral
KW - Adult
KW - Animals
KW - Blood Glucose
KW - Cell Line
KW - Cholecystokinin
KW - Dietary Carbohydrates
KW - Dose-Response Relationship, Drug
KW - Enteroendocrine Cells
KW - Female
KW - Fructose
KW - Gastric Inhibitory Polypeptide
KW - Glucagon
KW - Glucagon-Like Peptide 1
KW - Humans
KW - Insulin
KW - Intestines
KW - Ion Channel Gating
KW - KATP Channels
KW - Male
KW - Membrane Potentials
KW - Mice
KW - Mice, Inbred C57BL
KW - Rats
KW - Rats, Wistar
KW - Single-Blind Method
KW - Time Factors
KW - Young Adult
U2 - 10.1152/ajpgi.00372.2013
DO - 10.1152/ajpgi.00372.2013
M3 - Journal article
C2 - 24525020
VL - 306
SP - G622-30
JO - American Journal of Physiology: Gastrointestinal and Liver Physiology
JF - American Journal of Physiology: Gastrointestinal and Liver Physiology
SN - 0193-1857
IS - 7
ER -
ID: 117852315