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1.
Eur J Nutr ; 52(4): 1303-13, 2013 Jun.
Article in English | MEDLINE | ID: mdl-22926626

ABSTRACT

PURPOSE: Peptide YY (PYY) is a gastrointestinal hormone with physiological actions regulating appetite and energy homoeostasis. The cellular mechanisms by which nutrients stimulate PYY secretion from intestinal enteroendocrine cells are still being elucidated. METHODS: This study comprehensively evaluated the suitability of intestinal STC-1 cells as an in vitro model of PYY secretion. PYY concentrations (both intracellular and in culture media) with other intestinal peptides (CCK, GLP-1 and GIP) demonstrated that PYY is a prominent product of STC-1 cells. Furthermore, acute and chronic PYY responses to 15 short (SCFAs)- and long-chain (LCFAs) dietary fatty acids were measured alongside parameters for DNA synthesis, cell viability and cytotoxicity. RESULTS: We found STC-1 cells to be reliable secretors of PYY constitutively releasing PYY into cell culture media (but not into non-stimulatory buffer). We demonstrate for the first time that STC-1 cells produce PYY mRNA transcripts; that STC-1 cells produce specific time- and concentration-dependent PYY secretory responses to valeric acid; that linoleic acid and conjugated linoleic acid 9,11 (CLA 9,11) are potent PYY secretagogues; and that chronic exposure of SCFAs and LCFAs can be detrimental to STC-1 cells. CONCLUSIONS: Our studies demonstrate the potential usefulness of STC-1 cells as an in vitro model for investigating nutrient-stimulated PYY secretion in an acute setting. Furthermore, our discovery that CLA directly stimulates L-cells to secrete PYY indicates another possible mechanism contributing to the observed effects of dietary CLA on weight loss.


Subject(s)
Enterocytes/metabolism , Linoleic Acid/metabolism , Linoleic Acids, Conjugated/metabolism , Pentanoic Acids/metabolism , Peptide YY/metabolism , Secretory Pathway , Up-Regulation , Animals , Cell Line , Cell Survival , Cholecystokinin/metabolism , DNA Replication , Fatty Acids, Nonesterified/adverse effects , Fatty Acids, Nonesterified/metabolism , Fatty Acids, Volatile/adverse effects , Fatty Acids, Volatile/metabolism , Gastric Inhibitory Polypeptide/metabolism , Glucagon-Like Peptide 1/metabolism , Kinetics , Mice , Peptide YY/genetics , RNA, Messenger/metabolism
2.
Food Funct ; 3(11): 1131-43, 2012 Nov.
Article in English | MEDLINE | ID: mdl-22914860

ABSTRACT

The incidence of obesity and obesity-associated diseases, such as type-2 diabetes, has reached epidemic proportions in recent years. It is predicted that by 2015 over 1.5 billion consumers will be overweight or obese. Several of the current drug-based treatments on the market for weight management and appetite control either lack efficacy or are associated with adverse side-effects. There is, therefore, an opportunity to develop functional foods which are both nutritionally beneficial but which also aid in weight management. Peptides produced in the gastrointestinal tract, which function to regulate feed intake and satiety, have been identified as key targets for bioactive ingredients in functional foods. These peptides are produced and released by specialised enteroendocrine cells. Understanding the interaction of foods with these cells is vital to the development of food matrices with positive health benefits. This review describes enteroendocrine cell populations in detail and focuses on the peptides that they produce in addition to their other functions, including taste transduction. Several food-based sources of bioactives and current food products on the market with beneficial effects on satiety and glycaemia will also be discussed.


Subject(s)
Enteroendocrine Cells/metabolism , Gastrointestinal Hormones/metabolism , Gastrointestinal Tract , Peptide Hormones/metabolism , Signal Transduction/drug effects , Appetite Regulation , Glucagon-Like Peptide 1 , Glycemic Index , Humans , Incretins , Obesity/prevention & control , Satiation/physiology
3.
Food Nutr Res ; 562012.
Article in English | MEDLINE | ID: mdl-22509144

ABSTRACT

BACKGROUND: Starch is a main source of glucose and energy in the human diet. The extent to which it is digested in the gastrointestinal tract plays a major role in variations in postprandial blood glucose levels. Interactions with other biopolymers, such as dairy proteins, during processing can influence both the duration and extent of this postprandial surge. OBJECTIVE: To evaluate the effect of the addition of bovine α- or ß-casein to waxy maize starch on changes in postprandial blood glucose, insulin, and incretin hormones [glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1)] in 30 kg pigs used as an animal model for humans. DESIGN: Gelatinised starch, starch gelatinised with α-casein, and starch gelatinised with ß-casein were orally administered to trained pigs (n = 8) at a level of 60 g of available carbohydrate. Pre- and postprandial glucose measurements were taken every 15 min for the first hour and every 30 min thereafter up to 180 min. Insulin, GIP, and GLP-1 levels were measured in plasma samples up to 90 min postprandial. RESULTS: Starch gelatinised with α-casein had a significantly (p < 0.05) lower peak viscosity on pasting and resulted in significantly lower glucose release at 15, 30, and 90 min postprandial compared to starch gelatinised with ß-casein. During the first 45-min postprandial, the area under the glucose curve (AUC) for starch gelatinised with α-casein was significantly (p < 0.05) lower than that for starch gelatinised with ß-casein. There was also a significant (p < 0.05) difference at T30 in GIP levels in response to the control compared to starch gelatinised with α- or ß-casein. Significant (p < 0.05) increases in several free amino acid concentrations were observed on ingestion of either α- or ß-casein gelatinised with starch at 30 and 90 min postprandial compared to starch alone. In addition, plasma levels of six individual amino acids were increased on ingestion of starch gelatinised with α-casein compared to ingestion of starch gelatinised with ß-casein. CONCLUSION: The presence of casein fractions (α- or ß-casein) in gelatinised waxy maize starch affects swelling characteristics, viscosity, and subsequent in vivo digestion as determined by glucose levels in blood postprandial.

4.
Br J Nutr ; 107(2): 155-63, 2012 Jan.
Article in English | MEDLINE | ID: mdl-21733328

ABSTRACT

Foods that have a low glycaemic index or foods that contain slowly digestible starch are beneficial in controlling fluctuations in blood glucose and insulin levels. The study hypothesis is that gelatinisation of starch in structured casein networks provides a method for decreasing the digestion rate of the starch and, hence, minimising postprandial glucose fluctuations. This study examined the effect of starch gelatinisation with or without casein on (1) gene expression and peptide secretion levels of the incretin hormones glucagon-like peptide 1 and glucose-independent insulinotropic polypeptide and (2) gene expression of the sodium-glucose cotransporter and GLUT-2 in intestinal cell culture systems. The intestinal epithelial cell line, STC-1, and the enteroendocrine colonic cell line, Caco-2, were exposed to in vitro digested foods (starch gelatinised with α-casein, starch gelatinised with ß-casein and gelatinised starch alone). The encapsulation of starch with casein before in vitro digestion lowers levels of incretin hormone secretion. Digestion of starch gelatinised with casein also releases less glucose than starch alone as indicated by significantly (P < 0·05) lower levels of glucose transporter mRNA transcripts. Some subtle cellular response differences were observed following exposure to starch gelatinised with α- compared to ß-casein. Fractionation of α-casein and ß-casein by reverse-phase HPLC identified that fractions that differed in hydrophobicity differed significantly (P < 0·05) in their ability to promote secretion of the incretin hormones. Evidence suggests that gelatinisation of starch with casein may be a functional food ingredient that minimises blood glucose fluctuations.


Subject(s)
Enterocytes/metabolism , Incretins/metabolism , Monosaccharide Transport Proteins/metabolism , Starch/chemistry , Starch/metabolism , Animals , Caseins/chemistry , Caseins/metabolism , Cell Line , Digestion , Food, Formulated/analysis , Gastric Inhibitory Polypeptide/genetics , Gastric Inhibitory Polypeptide/metabolism , Gels , Gene Expression Regulation , Glucagon-Like Peptide 1/genetics , Glucagon-Like Peptide 1/metabolism , Glucose/metabolism , Glucose Transporter Type 2/genetics , Glucose Transporter Type 2/metabolism , Humans , Incretins/genetics , Intestinal Absorption , Mice , Protein Hydrolysates/chemistry , Protein Hydrolysates/metabolism , Protein Isoforms/chemistry , Protein Isoforms/metabolism , RNA, Messenger/metabolism , Sodium-Glucose Transporter 1/genetics , Sodium-Glucose Transporter 1/metabolism
5.
Mol Nutr Food Res ; 54 Suppl 1: S93-S103, 2010 May.
Article in English | MEDLINE | ID: mdl-20352619

ABSTRACT

Cholecystokinin (CCK) is a peptide hormone secreted from the I-cells of the intestine and it has important physiological actions related to appetite regulation and satiety. In this study we used STC-1 cells to investigate the effects of common dietary-derived fatty acids (FAs) on I-cell secretory function and metabolism. We extend earlier studies by measuring the acute and chronic effects of 11 FAs on CCK secretion, cellular CCK content, CCK mRNA levels, cellular DNA synthesis, cellular viability and cytotoxicity. FAs were selected in order to assess the importance of chain length, degree of saturation, and double bond position and conformation. The results demonstrate that secretory responses elicited by dietary FAs are highly selective. For example, altering the conformation of a double bond from cis to trans (i.e. oleic acid versus elaidic acid) completely abolishes CCK secretion. Lauric acid appears to adversely affect I-cell metabolism and arachidonic acid suppresses DNA synthesis. Our studies reveal for the first time that conjugated linoleic acid isoforms are particularly potent CCK secretagogues, which also boost intracellular stores of CCK. These actions of conjugated linoleic acid may explain satiating actions observed in dietary intervention studies.


Subject(s)
Cholecystokinin/genetics , Dietary Fats/pharmacology , Animals , Cell Line, Tumor , Cell Survival/drug effects , Cholecystokinin/drug effects , Cholecystokinin/metabolism , DNA Primers , DNA Replication/drug effects , Fatty Acids/pharmacology , Gene Expression Regulation, Neoplastic , Mice , Mice, Transgenic , RNA, Messenger/genetics , RNA, Neoplasm/genetics
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