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B Messenger, MN Clifford and LM Morgan

Gastrointestinal peptides, including insulin, glucagon and glucose-dependent insulinotropic polypeptide (GIP) have previously been reported in salivary glands. Recent evidence has suggested they might influence postprandial macronutrient metabolism. This study therefore investigated and compared postprandial hormone concentrations in saliva and plasma to determine whether their secretion was influenced by oral food stimuli. In a within-subject randomised cross-over comparison of hormone concentrations in plasma and saliva following a mixed meal, 12 subjects were given two 1708 kJ mixed meals. On one occasion the meal was chewed and swallowed (swallowed meal), on the other it was chewed and expectorated (sham-fed meal). Salivary and plasma levels of immunoreactive insulin, GIP and glucagon-like peptide-1 (GLP-1), total protein, alpha-amylase, glucose and non-esterified fatty acid were measured before and for 90 min following the meals. Saliva total protein and alpha-amylase rose following both meals, indicating that the stimulus for salivary protein release is related to the presence of food in the mouth. GLP-1 was not detected in saliva. Fasting salivary insulin levels were lower in saliva than plasma (28+/-6 vs 40+/-25 pmol/l respectively). Both increased following the swallowed meal but the rise in saliva was slower and less marked than in plasma (peak levels 96+/-18 and 270+/-66 pmol/l for saliva and plasma respectively, P<0.01). Both were unchanged following the sham-fed meal. GIP was detected in saliva. Fasting GIP levels were significantly higher in saliva than plasma (183+/-23 compared with 20+/-7 pmol/l, P<0.01). They decreased in saliva following both swallowed and sham-fed meals to nadirs of 117+/-17 and 71+/-12 pmol/l respectively, but rose following the swallowed meal to peak levels of 268+/-66 pmol/l. These findings are consistent with insulin in saliva being an ultrafiltrate of that circulating in blood, but GIP in saliva being the product of local salivary gland synthesis, whose secretion is influenced, directly or indirectly, by oral stimuli. The function of salivary GIP is unknown, but we speculate that it may play a role in the regulation of gastric acid secretion in the fasting state.

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S J Brandt, M Kleinert, M H Tschöp and T D Müller

). For example, following Roux-en-Y gastric bypass, gastric banding or sleeve gastronomy, there is an increase in the secretion of glucagon-like peptide 1 (GLP-1) ( Laferrere 2016 , Meek et al. 2016 , Clemmensen et al. 2017 ), which is known not

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Paige V Bauer and Frank A Duca

. 2015 , Buse et al . 2016 ). Interestingly, this is not the only evidence for a therapeutic role of the gut in diabetes treatment. Over the past decade, incretin-based therapies including glucagon-like peptide-1 (GLP-1) receptor agonists and dipeptidyl

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Bethany P Cummings, Andrew A Bremer, Timothy J Kieffer, David D'Alessio and Peter J Havel

hypothesized that dexamethasone may enhance postprandial insulin secretion by increasing meal-stimulated incretin hormone secretion and/or by increasing parasympathetic input to the pancreas. The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose

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Jacob Jelsing, Niels Vrang, Søren B van Witteloostuijn, Michael Mark and Thomas Klein

Introduction The incretin hormone glucagon-like peptide 1 (GLP1) is a gut peptide that is secreted in response to nutrient ingestion. It enhances the glucose-dependent stimulation of insulin secretion and also controls blood glucose (BG) via

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Shin Tsunekawa, Naoki Yamamoto, Katsura Tsukamoto, Yuji Itoh, Yukiko Kaneko, Toshihide Kimura, Yoh Ariyoshi, Yoshitaka Miura, Yutaka Oiso and Ichiro Niki

Introduction The beneficial effects of glucagon-like peptide 1 (GLP-1) and its related substances such as inhibitors of dipeptidyl peptidase IV, its degrading enzyme, on the pancreatic β-cells have been reported; these agents enhance

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Hiranya Pintana, Nattayaporn Apaijai, Nipon Chattipakorn and Siriporn C Chattipakorn

al . 2010 ). In this context, anti-diabetic agents such as rosiglitazone and glucagon-like peptide (GLP-1) have been reported to negate cognitive decline ( During et al . 2003 , Escribano et al . 2009 , Wang et al . 2011 ). Recently developed

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Bethany P Cummings, Ahmed Bettaieb, James L Graham, Kimber Stanhope, Fawaz G Haj and Peter J Havel

peroxisome proliferator receptor γ (PPARγ) and glucagon-like peptide 1 (GLP1). PPARγ is a nuclear receptor that is highly expressed in adipose tissue and macrophages and acts to upregulate the expression of factors involved in adipocyte differentiation and

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Neil Tanday, Peter R Flatt, Nigel Irwin and R Charlotte Moffett

incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), in T2DM have been linked to direct positive effects at the level of the endocrine pancreas. This includes, but not limited to, potentiation of glucose

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Hidetada Ogata, Yusuke Seino, Norio Harada, Atsushi Iida, Kazuyo Suzuki, Takako Izumoto, Kota Ishikawa, Eita Uenishi, Nobuaki Ozaki, Yoshitaka Hayashi, Takashi Miki, Nobuya Inagaki, Shin Tsunekawa, Yoji Hamada, Susumu Seino and Yutaka Oiso

Introduction Incretins, the gut hormones such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP1), which are secreted from enteroendocrine K-cells and L-cells, respectively, following meal ingestion stimulate