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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.
Department of Cell Biology, Physiology and Immunology, Universitat Autonòma de Barcelona, Bellaterra 08193, Spain
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Department of Cell Biology, Physiology and Immunology, Universitat Autonòma de Barcelona, Bellaterra 08193, Spain
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Department of Cell Biology, Physiology and Immunology, Universitat Autonòma de Barcelona, Bellaterra 08193, Spain
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Department of Cell Biology, Physiology and Immunology, Universitat Autonòma de Barcelona, Bellaterra 08193, Spain
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Department of Cell Biology, Physiology and Immunology, Universitat Autonòma de Barcelona, Bellaterra 08193, Spain
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related to the fatty acid composition of membrane phospholipids, which in turn is influenced by dietary PUFA intake and metabolism ( Lands 1989 ). In gilthead sea bream, dietary deficiencies on n-3 HUFA, essential fatty acids for marine fish
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Abstract
This study was designed to investigate postprandial responses to a mixed meal in simulated shift work conditions. Nine normal healthy subjects (six males and three females) were studied on two occasions at the same clock time (1330 h) after consuming test meals, first in their normal environment and secondly after a 9 h phase advance (body clock time 2230 h). Plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), triacylglycerol (TAG) and non-esterified fatty acids (NEFAs) were determined at intervals for 6 h after each test meal. Postprandial plasma glucose, insulin, GIP and GLP-1 profiles were evaluated by calculating areas under the curve (AUC) for the first 2 h and the last 4 h of the sampling together with total AUC. Significantly higher postprandial glucose responses (total AUC) were observed after the phase shift than before (AUC 0–360 min, 2·01 (1·51–2·19) vs 1·79 (1·56–2·04) mmol/l.min; P<0·02; mean (range)). No significant difference was observed when the first 2 h of each response was compared, but significantly higher glucose levels were observed in the last 4 h of the study after the phase shift than before (AUC 120–360 min, 1·32 (1·08–1·42) vs 1·16 (1·00–1·28) mmol/l.min; P<0·05). Similar results were obtained for insulin (AUC 0—360 min, 81·72 (30·75– 124·97) vs 58·98 (28·03–92·57) pmol/l.min; P<0·01; AUC 120–360 min, 40·73 (16·20–65·25) vs 25·71 (14·25–37·33) pmol/l.min; P<0·02). No differences were observed in postprandial plasma GIP and GLP-1 responses before and after the phase shift. Postprandial circulating lipid levels were affected by phase shifting. Peak plasma TAG levels occurred 5 h postprandially before the phase shift. Postprandial rises in plasma TAG were significantly delayed after the phase shift and TAG levels continued to rise throughout the study. Plasma postprandial NEFA levels fell during the first 3 h both before and after the phase shift. Their rate of return to basal levels was significantly delayed after the phase shift compared with before. This study demonstrates that a simulated phase shift can significantly alter pancreatic B-cell responses and postprandial glucose and lipid metabolism.
Journal of Endocrinology (1996) 151, 259–267
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metabolism and promote lipid mobilization ( Izumida et al. 2013 ). To better clear circulating fatty acids, the liver upregulates expression of the hepatic fatty acid transporter Cd36 ( Xu et al. 2013 ). In the mouse, significant accumulation of hepatic
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protection against inflammation-impaired insulin secretion ( Clark 2002 ). Induction of adipokines Adiponectin is one of the adipokines most abundantly produced by adipose tissue and is a key regulator of fatty acid and glucose metabolism ( Karbowska & Kochan
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lower levels in HFRD rats. By comparing SD and HFRD rats at the 0-min time point, differences were identified for various compounds, including phospholipids, amino acids, bile acids, fatty acids and metabolites. Moreover, regarding purine metabolism and
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Abstract
The effect of body condition per se on plasma IGFs and IGF-binding proteins (IGFBPs) and the whole-body metabolic responses to recombinant DNA-derived bovine GH (rbGH) in both the fed and the fasted state were determined in lean and dietary obese sheep (n=6/group). Sheep at zero-energy balance and equilibrium body weight were injected s.c. for 12 days with 100 μg/kg rbGH immediately before their morning feeding. Before GH treatment, fasting plasma concentrations of insulin (17·0 ± 1·9 vs 7·5 ± 0·7 μU/ml), IGF-I (345 ± 25 vs 248 ± 10 ng/ml), glucose (52·6 ± 1·1 vs 48·3 ± 0·7 mg/dl), and free fatty acid (FFA) (355 ± 45 vs 229 ± 24 nmol/ml) were greater (P<0·05) and those of GH (1·1 ± 0·2 vs 2·6 ± 0·3 ng/ml) were lower (P<0·05) in obese than in lean sheep. Fasting concentrations of IGF-II and glucagon were not affected (P>0·05) by obesity. GH concentrations were increased equivalently by 6–9 ng/ml in lean and obese sheep during GH treatment. GH caused an immediate and a marked fivefold increase in the fasting insulin level in obese sheep but only minimally affected insulin concentration in lean sheep. The increment in fasting glucose during GH treatment was greater (P<0·05) in obese (8–12 mg/dl) than in lean (2–5 mg/dl) sheep. Frequent measurements in the first 8 h after feeding and injection of excipient (day 0) or the first (day 1), sixth (day 6) and twelfth (day 12) daily injection of GH showed that prandial metabolism in both groups of sheep was affected minimally by GH. However, GH treatment on day 1 (not days 6 or 12) acutely attenuated the feeding-induced suppression of plasma FFA in both groups of sheep and this effect was significantly greater in obese than in lean sheep.
Although obese sheep were hyposomatotropic, the basal and GH-induced increases in plasma IGF-I concentrations were greater (P<0·05) in obese than in lean sheep. Plasma IGF-II was unaffected by obesity and was not increased by GH stimulation. Western ligand blotting showed that IGFBP-3 accounted for approximately 50–60% of the plasma IGF-I binding capacity in sheep respectively both before and during GH treatment. Basal plasma levels of IGFBP-2 were lower (P<0·05) and those of IGFBP-3 greater (P<0·05) in obese compared with lean sheep. GH increased the level of IGFBP-3 equally in lean and obese sheep, but suppressed the expression of IGFBP-2 more (P<0·05) in lean than in obese sheep. We concluded that the diabetogenic-like actions of GH in sheep were exaggerated markedly by obesity, and were expressed more during the fasted than the fed states. The effects of GH stimulation on the endocrine pancreas may be selective for β-cells and preferentially enhanced by obesity. GH regulation of IGF-I and the IGFBPs differs in lean and obese sheep.
Journal of Endocrinology (1997) 154, 329–346
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Division of Diabetes, Endocrinology, & Metabolism, Vanderbilt University Medical Center School of Medicine, Nashville, Tennessee, USA
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preferentially utilise other substrates to maintain the energy production needed for glucagon secretion. Fatty acid metabolism and the regulation of glucagon secretion Oxidation of fatty acids Metabolic flexibility allows most cells to utilise
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. Endocrinology and Metabolism 280 E788 – E796 . Stein DT Esser V Stevenson BE Lane KE Whiteside JH Daniels MB Chen S McGarry JD 1996 Essentiality of circulating fatty acids for glucose-stimulated insulin secretion in the fasted rat . Journal of
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response to chronically elevated free fatty acids in pancreatic β-cells . American Journal of Physiology. Endocrinology and Metabolism 294 E540 – E550 . Laybutt DR Preston AM Akerfeldt MC Kench JG Busch AK Biankin AV Biden TJ 2007 Endoplasmic
