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Differential impact of a ghrelin receptor antagonist or inverse agonist in the electrical kindling model of epilepsy

Beheshti S, Ershadi S, Zamani F, Azimzadeh M, Wesal MW

Epilepsy Res, 2023 Nov;197:107234.
PMID: 37793283 DOI: 10.1016/j.eplepsyres.2023.107234

Ghrelin is a peptide, which has been shown to affect seizures. However, there is not a consensus about its real impact on the control of seizure severity. We assessed the influence of intra-amygdala injections of a ghrelin receptor (GHSR) antagonist, as well as a GHSR inverse agonist on the electrical kindling-induced seizures. Two unipolar electrodes and a tripolar electrode twisted with a guide cannula were implanted in the skull surface or the basolateral amygdala of adult male rats, respectively. A rapid electrical kindling protocol was applied for kindling epileptogenesis. The stimulations were applied until rats showed three consecutive stage five seizures. Each rat was considered as its control. D-Lys-3-GHRP-6 (1, 12.5, and 25 μg/rat) or [D-Arg, D-phe, D-Trp, heu] substance P (D-SP) (50, 500 and 5000 ng/rat) as the GHSR antagonist or inverse agonist were injected into the basolateral amygdala. Seizure parameters including after-discharge duration (ADD), stage five duration (S5D), and seizure stage (SS) were documented thirty minutes following administration of the drugs or saline. Antagonism of the GHSR in the amygdala, significantly increased seizure induction in the kindled rats, in a dose-dependent manner, and induced spontaneous seizures leading to status epilepticus. Conversely, D-SP had a dose-dependent anticonvulsant activity, indicated by decreased ADD and S5D. The results show that GHSR inverse agonism suppressed seizure severity in the rat amygdala kindling model, whereas GHSR antagonism made seizures more severe. Therefore, when considering the ghrelin system to modulate seizures, it is crucial to note the differential impact of various GHSR ligands.

Matched MeSH terms: Ghrelin/pharmacology; Receptors, Ghrelin
Blood Profile, Hormones, and Telomere Responses: Potential Biomarkers in Horses Exhibiting Abnormal Oral Behavior

Hanis F, Chung ELT, Kamalludin MH, Idrus Z

J Equine Vet Sci, 2022 Nov;118:104130.
PMID: 36182046 DOI: 10.1016/j.jevs.2022.104130

The high prevalence of abnormal oral behavior (AOB) in working horses has been linked to management issues and the pathophysiology of this behavior remains unclear. Therefore, this study aims to elucidate the blood profile, hormones, and telomere length responses between low and high levels of AOB among different horse working groups. A total of 207 healthy horses from various breeds were initially selected from four working groups (leisure riding, equestrian, endurance, and patrolling) and observed for the time spent on AOB. Then, six horses each with higher and lower AOB than the population means were randomly selected from each of the working groups and categorized as high and low AOB horses, respectively. Blood samples were collected for hematology, biochemistry, cortisol, ghrelin, leptin, and relative telomere length analyzes. High AOB horses notably had higher values of glucose, alanine aminotransferase (ALT), alkaline phosphatase (ALP), and creatine kinase (CK) compared to low AOB horses. High AOB horses also recorded higher plasma cortisol and ghrelin, but lower leptin concentrations. Among working groups, both endurance and patrolling horses presented the highest values in sodium, potassium, chloride, phosphate, ALT, and CK. While patrolling horses had the lowest levels of urea, ALP, and albumin levels, equestrian and leisure horses recorded the highest and lowest plasma cortisol and leptin concentrations, respectively. Finally, the telomere length of endurance and patrolling horses were significantly greater than leisure and equestrian horses. The present findings suggest that AOB horses had distinctive physiological characteristics that could be linked to improper diet and a demanding workload, while ghrelin and leptin hormones could be potential biomarkers for this behavior.

Matched MeSH terms: Ghrelin*
AgRP/NPY and POMC neurons in the arcuate nucleus and their potential role in treatment of obesity

Vohra MS, Benchoula K, Serpell CJ, Hwa WE

Eur J Pharmacol, 2022 Jan 15;915:174611.
PMID: 34798121 DOI: 10.1016/j.ejphar.2021.174611

Obesity is a major health crisis affecting over a third of the global population. This multifactorial disease is regulated via interoceptive neural circuits in the brain, whose alteration results in excessive body weight. Certain central neuronal populations in the brain are recognised as crucial nodes in energy homeostasis; in particular, the hypothalamic arcuate nucleus (ARC) region contains two peptide microcircuits that control energy balance with antagonistic functions: agouti-related peptide/neuropeptide-Y (AgRP/NPY) signals hunger and stimulates food intake; and pro-opiomelanocortin (POMC) signals satiety and reduces food intake. These neuronal peptides levels react to energy status and integrate signals from peripheral ghrelin, leptin, and insulin to regulate feeding and energy expenditure. To manage obesity comprehensively, it is crucial to understand cellular and molecular mechanisms of information processing in ARC neurons, since these regulate energy homeostasis. Importantly, a specific strategy focusing on ARC circuits needs to be devised to assist in treating obese patients and maintaining weight loss with minimal or no side effects. The aim of this review is to elucidate the recent developments in the study of AgRP-, NPY- and POMC-producing neurons, specific to their role in controlling metabolism. The impact of ghrelin, leptin, and insulin signalling via action of these neurons is also surveyed, since they also impact energy balance through this route. Lastly, we present key proteins, targeted genes, compounds, drugs, and therapies that actively work via these neurons and could potentially be used as therapeutic targets for treating obesity conditions.

Matched MeSH terms: Ghrelin/metabolism
Extragastrointestinal manifestations of Helicobacter pylori infection: facts or myth? A critical review

Tan HJ, Goh KL

J Dig Dis, 2012 Jul;13(7):342-9.
PMID: 22713083 DOI: 10.1111/j.1751-2980.2012.00599.x

Helicobacter pylori (H. pylori) infection is reported to be associated with many extragastrointestinal manifestations, such as hematological diseases [idiopathic thrombocytopenic purpura (ITP) and unexplained iron deficiency anemia (IDA)], cardiovascular diseases (ischemic heart diseases), neurological disorders (stroke, Parkinson's disease, Alzheimer's disease), obesity and skin disorders. Among these, the best evidence so far is in ITP and unexplained IDA, with high-quality studies showing the improvement of IDA and ITP after H. pylori eradication. The evidence of its association with coronary artery disease is weak and many of the results may be erroneous. The role of H. pylori infection in affecting serum leptin and ghrelin levels has attracted a lot of attention recently and available data to date have been conflicting. There have also been many uncontrolled, small sample studies suggesting an association between H. pylori infection and neurological disorders or chronic urticaria. However, more studies are required to clarify such proposed causal links.

Matched MeSH terms: Ghrelin/blood
Fulltext Helicobacter pylori and gut microbiota modulate energy homeostasis prior to inducing histopathological changes in mice

Khosravi Y, Bunte RM, Chiow KH, Tan TL, Wong WY, Poh QH, et al.

Gut Microbes, 2016;7(1):48-53.
PMID: 26939851 DOI: 10.1080/19490976.2015.1119990

Helicobacter pylori have been shown to influence physiological regulation of metabolic hormones involved in food intake, energy expenditure and body mass. It has been proposed that inducing H. pylori-induced gastric atrophy damages hormone-producing endocrine cells localized in gastric mucosal layers and therefore alter their concentrations. In a recent study, we provided additional proof in mice under controlled conditions that H. pylori and gut microbiota indeed affects circulating metabolic gut hormones and energy homeostasis. In this addendum, we presented data from follow-up investigations that demonstrated H. pylori and gut microbiota-associated modulation of metabolic gut hormones was independent and precedes H. pylori-induced histopathological changes in the gut of H. pylori-infected mice. Thus, H. pylori-associated argumentation of energy homeostasis is not caused by injury to endocrine cells in gastric mucosa.

Matched MeSH terms: Ghrelin/metabolism
Fulltext Effect of Sequence of Fruit Intake in a Meal on Satiety

Abdul Hakim BN, Yahya HM, Shahar S, Abdul Manaf Z, Damanhuri H

Int J Environ Res Public Health, 2019 11 13;16(22).
PMID: 31766283 DOI: 10.3390/ijerph16224464

Little is known about the effects of manipulating sequence of fruit consumption during a meal in suppressing an individual's appetite. Therefore, we investigate the effects of the sequence of fruit intake on satiety and blood glucose in a group of 17 healthy, young male adults. This intervention study repeatedly measured the effects of fruit intake (120 g red apple) before and after a meal and control (no fruit). Ad libitum test meal was weighed before and after a meal. Subjective appetite rating and appetite-related hormones were assessed at regular time intervals. The satiety score was significantly higher for fruit intake before a meal followed by after a meal and control (p < 0.05). Eating fruit before a meal reduced 18.5% (166 kcal) subsequent energy intake compared to control (p < 0.05). Fruit intake before a meal had a significantly higher incremental area under the curve (iAUC) of Glucagon-like peptide 1 (GLP-1), compared to after a meal (p < 0.05). There were no differences in plasma changes of ghrelin, Cholecystokinin 8 (CCK8), or blood glucose in all sessions. Consuming fruit before a meal potentially enhanced satiety. Further research is required to confirm both short- and long-term effects of the sequence of fruit intake on appetite regulation in a wider population.

Matched MeSH terms: Ghrelin/blood
Fulltext Central pathways integrating metabolism and reproduction in teleosts

Shahjahan M, Kitahashi T, Parhar IS

Front Endocrinol (Lausanne), 2014;5:36.
PMID: 24723910 DOI: 10.3389/fendo.2014.00036

Energy balance plays an important role in the control of reproduction. However, the cellular and molecular mechanisms connecting the two systems are not well understood especially in teleosts. The hypothalamus plays a crucial role in the regulation of both energy balance and reproduction, and contains a number of neuropeptides, including gonadotropin-releasing hormone (GnRH), orexin, neuropeptide-Y, ghrelin, pituitary adenylate cyclase-activating polypeptide, α-melanocyte stimulating hormone, melanin-concentrating hormone, cholecystokinin, 26RFamide, nesfatin, kisspeptin, and gonadotropin-inhibitory hormone. These neuropeptides are involved in the control of energy balance and reproduction either directly or indirectly. On the other hand, synthesis and release of these hypothalamic neuropeptides are regulated by metabolic signals from the gut and the adipose tissue. Furthermore, neurons producing these neuropeptides interact with each other, providing neuronal basis of the link between energy balance and reproduction. This review summarizes the advances made in our understanding of the physiological roles of the hypothalamic neuropeptides in energy balance and reproduction in teleosts, and discusses how they interact with GnRH, kisspeptin, and pituitary gonadotropins to control reproduction in teleosts.

Matched MeSH terms: Ghrelin
Expression of neuropeptide Y and gonadotropin-releasing hormone gene types in the brain of female Nile tilapia (Oreochromis niloticus) during mouthbrooding and food restriction

Das K, Ogawa S, Kitahashi T, Parhar IS

Peptides, 2019 02;112:67-77.
PMID: 30389346 DOI: 10.1016/j.peptides.2018.10.009

A cichlid fish, the Nile tilapia (Oreochromis niloticus), is a maternal mouthbrooder, which exhibits minimum energy expenditure and slower ovarian cycles during mouthbrooding. The objective of this study was to observe changes in the gene expression of key neuropeptides involved in the control of appetite and reproduction, including neuropeptide Y a (NPYa), reproductive neuropeptides: gonadotropin-releasing hormone (GnRH1, GnRH2 and GnRH3) and kisspeptin (Kiss2) during mouthbrooding (4- and 12-days), 12-days of food restriction and 12-days of food restriction followed by refeeding. The food restriction regime showed a significant increase in npya mRNA levels in the telencephalon. However, there were no significant alterations in npya mRNA levels during mouthbrooding. gnrh1 mRNA levels were significantly lower in mouthbrooding female as compared with females with food restriction. gnrh3 mRNA levels were also significantly lower in female with 12-days of mouthbrooding, 12-days of food restriction followed by 12-days of refeeding when compared with controls. There were no significant differences in gnrh2 and kiss2 mRNA levels between groups under different feeding regimes. No significant changes were observed in mRNA levels of receptors for peripheral metabolic signaling molecules: ghrelin (GHS-R1a and GHS-R1b) and leptin (Lep-R). These results suggested that unaffected npya mRNA levels in the telencephalon might contribute to suppression of appetite in mouthbrooding female tilapia. Furthermore, lower gnrh1 and gnrh3 mRNA levels may influence the suppression of reproductive functions such as progression of ovarian cycle and reproductive behaviours, while GnRH2 and Kiss2 may not play a significant roles in reproduction under food restriction condition.

Matched MeSH terms: Ghrelin/genetics
The role of leptin and ghrelin in appetite regulation in the Australian Spinifex hopping mouse, Notomys alexis, during long-term water deprivation

Donald JA, Hamid NKA, McLeod JL

Gen Comp Endocrinol, 2017 04 01;244:201-208.
PMID: 27102941 DOI: 10.1016/j.ygcen.2016.04.015

Water deprivation of the Spinifex hopping mouse, Notomys alexis, induced a biphasic pattern of food intake with an initial hypophagia that was followed by an increased, and then sustained food intake. The mice lost approximately 20% of their body mass and there was a loss of white adipose tissue. Stomach ghrelin mRNA was significantly higher at day 2 of water deprivation but then returned to the same levels as water-replete (day 0) mice for the duration of the experiment. Plasma ghrelin was unaffected by water deprivation except at day 10 where it was significantly increased. Plasma leptin levels decreased at day 2 and day 5 of water deprivation, and then increased significantly by the end of the water deprivation period. Water deprivation caused a significant decrease in skeletal muscle leptin mRNA expression at days 2 and 5, but then it returned to day 0 levels by day 29. In the hypothalamus, water deprivation caused a significant up-regulation in both ghrelin and neuropeptide Y mRNA expression, respectively. In contrast, hypothalamic GHSR1a mRNA expression was significantly down-regulated. A significant increase in LepRb mRNA expression was observed at days 17 and 29 of water deprivation. This study demonstrated that the sustained food intake in N. alexis during water deprivation was uncoupled from peripheral appetite-regulating signals, and that the hypothalamus appears to play an important role in regulating food intake; this may contribute to the maintenance of fluid balance in the absence of free water.

Matched MeSH terms: Ghrelin/metabolism*
Fulltext Helicobacter pylori infection can affect energy modulating hormones and body weight in germ free mice

Khosravi Y, Seow SW, Amoyo AA, Chiow KH, Tan TL, Wong WY, et al.

Sci Rep, 2015;5:8731.
PMID: 25736205 DOI: 10.1038/srep08731

Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.

Matched MeSH terms: Ghrelin/metabolism
Fulltext Asperuloside Enhances Taste Perception and Prevents Weight Gain in High-Fat Fed Mice

Ishaq M, Tran D, Wu Y, Nowak K, Deans BJ, Xin JTZ, et al.

Front Endocrinol (Lausanne), 2021;12:615446.
PMID: 33927690 DOI: 10.3389/fendo.2021.615446

Asperuloside is an iridoid glycoside found in many medicinal plants that has produced promising anti-obesity results in animal models. In previous studies, three months of asperuloside administration reduced food intake, body weight, and adipose masses in rats consuming a high fat diet (HFD). However, the mechanisms by which asperuloside exerts its anti-obesity properties were not clarified. Here, we investigated homeostatic and nutrient-sensing mechanisms regulating food intake in mice consuming HFD. We confirmed the anti-obesity properties of asperuloside and, importantly, we identified some mechanisms that could be responsible for its therapeutic effect. Asperuloside reduced body weight and food intake in mice consuming HFD by 10.5 and 12.8% respectively, with no effect on mice eating a standard chow diet. Fasting glucose and plasma insulin were also significantly reduced. Mechanistically, asperuloside significantly reduced hypothalamic mRNA ghrelin, leptin, and pro-opiomelanocortin in mice consuming HFD. The expression of fat lingual receptors (CD36, FFAR1-4), CB1R and sweet lingual receptors (TAS1R2-3) was increased almost 2-fold by the administration of asperuloside. Our findings suggest that asperuloside might exert its therapeutic effects by altering nutrient-sensing receptors in the oral cavity as well as hypothalamic receptors involved in food intake when mice are exposed to obesogenic diets. This signaling pathway is known to influence the subtle hypothalamic equilibrium between energy homeostasis and reward-induced overeating responses. The present pre-clinical study demonstrated that targeting the gustatory system through asperuloside administration could represent a promising and effective new anti-obesity strategy.

Matched MeSH terms: Ghrelin/metabolism
Fulltext Enhanced Contextual Fear Memory and Elevated Astroglial Glutamate Synthase Activity in Hippocampal CA1 BChE shRNA Knockdown Mice

Chen S, Lin Z, Tan KL, Chen R, Su W, Zhao H, et al.

Front Psychiatry, 2020;11:564843.
PMID: 33061920 DOI: 10.3389/fpsyt.2020.564843

Butyrylcholinesterase (BChE) efficiently hydrolyzes acetylcholine (ACh) at high concentrations when acetylcholinesterase (AChE) is substrate-inhibited. Recent studies have shown that BChE also has a function that is independent of ACh, but it has not been fully explored. Low BChE expression is accompanied with higher stress-induced aggression and ghrelin levels in stress models, and BChE knockout mice exhibit cognitive and memory impairments. However, the role of BChE in posttraumatic stress disorder (PTSD) remains unclear. In the present study, we investigated the role of BChE in contextual fear memory and its regulatory effect on the expression of factors related to the glutamate (Glu)-glutamine (Gln) cycle via knockdown studies. We used AAVs and lentiviruses to knockdown BChE expression in the mouse hippocampal CA1 region and C8D1A astrocytes. Our behavioral data from those mice injected with AAV-shBChE in the hippocampal CA1 region showed strengthened fear memory and increased dendritic spine density. Elevated Glu levels and glutamine synthetase (GS) enzyme activity were detected in contextual fear conditioned-BChE knockdown animals and astrocytes. We observed that an AAV-shBChE induced lowering of BChE expression in the hippocampus CA1 region enhanced contextual fear memory expression and promoted the astrocytic Glu-Gln cycle but did not elevate ACh-hydrolyzing activity. This study provides new insight into the regulatory role of BChE in cognition and suggests potential target for stress-related psychiatric disorder such as PTSD where patients experience fear after exposure to severe life-threatening traumatic events.

Matched MeSH terms: Ghrelin
Butyrylcholinesterase: A Multifaceted Pharmacological Target and Tool

Ha ZY, Mathew S, Yeong KY

Curr Protein Pept Sci, 2020;21(1):99-109.
PMID: 31702488 DOI: 10.2174/1389203720666191107094949

Butyrylcholinesterase is a serine hydrolase that catalyzes the hydrolysis of esters in the body. Unlike its sister enzyme acetylcholinesterase, butyrylcholinesterase has a broad substrate scope and lower acetylcholine catalytic efficiency. The difference in tissue distribution and inhibitor sensitivity also points to its involvement external to cholinergic neurotransmission. Initial studies on butyrylcholinesterase showed that the inhibition of the enzyme led to the increment of brain acetylcholine levels. Further gene knockout studies suggested its involvement in the regulation of amyloid-beta, a brain pathogenic protein. Thus, it is an interesting target for neurological disorders such as Alzheimer's disease. The substrate scope of butyrylcholinesterase was recently found to include cocaine, as well as ghrelin, the "hunger hormone". These findings led to the development of recombinant butyrylcholinesterase mutants and viral gene therapy to combat cocaine addiction, along with in-depth studies on the significance of butyrylcholinesterase in obesity. It is observed that the pharmacological impact of butyrylcholinesterase increased in tandem with each reported finding. Not only is the enzyme now considered an important pharmacological target, it is also becoming an important tool to study the biological pathways in various diseases. Here, we review and summarize the biochemical properties of butyrylcholinesterase and its roles, as a cholinergic neurotransmitter, in various diseases, particularly neurodegenerative disorders.

Matched MeSH terms: Ghrelin/antagonists & inhibitors; Ghrelin/genetics; Ghrelin/metabolism
Ghrelin stimulates growth hormone release from the pituitary via hypothalamic growth hormone-releasing hormone neurons in the cichlid, Oreochromis niloticus

Ogawa S, Liu X, Shepherd BS, Parhar IS

Cell Tissue Res, 2018 Nov;374(2):349-365.
PMID: 29934855 DOI: 10.1007/s00441-018-2870-6

Ghrelin, a gut-brain peptide hormone, is implicated in a multiplicity of biological functions, including energy homeostasis and reproduction. Neuronal systems that are involved in energy homeostasis as well as reproduction traverse the hypothalamus; however, the mechanism by which they control energy homeostasis is not fully understood. The present study analyzes the anatomical relationship of neurons expressing gonadotropin-releasing hormone (GnRH), neuropeptide Y (NPY) and growth hormone-releasing hormone (GHRH) in a cichlid, tilapia (Oreochromis niloticus). Additionally, we examine in vivo effects of ghrelin on these hypothalamic neurons and plasma growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels. Double-immunofluorescence showed neuronal fiber associations between GnRH, NPY and GHRH in the brain and pituitary. Intracerebroventricular injection of ghrelin had no effect on numbers, soma size, or optical density of GnRH and NPY neurons, whereas the number of GHRH neurons was significantly decreased in the animals injected with ghrelin when compared to controls, which may indicate administered ghrelin promoted GHRH release. Plasma GH and pituitary GH mRNA levels were significantly increased in the animals injected with ghrelin. These results suggest that central administration of ghrelin primarily act on hypothalamic GHRH neurons to stimulate GH release from the pituitary in the tilapia.

Matched MeSH terms: Ghrelin
Improvement in binge eating in non-diabetic obese individuals after 3 months of treatment with liraglutide - A pilot study

Robert SA, Rohana AG, Shah SA, Chinna K, Wan Mohamud WN, Kamaruddin NA

Obes Res Clin Pract, 2015 May-Jun;9(3):301-4.
PMID: 25870084 DOI: 10.1016/j.orcp.2015.03.005

We examined the effects of liraglutide, a glucagon-like peptide-1 analogue on appetite and plasma ghrelin in non-diabetic obese participants with subclinical binge eating (BE). Forty-four obese BE participants (mean age: 34±9 years, BMI: 35.9±4.2kg/m(2)) were randomly assigned to intervention or control groups for 12 weeks. All participants received standard advice for diet and exercise. Binge eating score, ghrelin levels and other anthropometric variables were evaluated at baseline and at the end of the study. Participants who received liraglutide showed significant improvement in binge eating, accompanied by reduction in body weight, BMI, waist circumference, systolic blood pressure, fasting glucose and total cholesterol. Ghrelin levels were significantly increased which may potentially diminish the weight loss effects of liraglutide beyond the intervention.

Matched MeSH terms: Ghrelin/blood
The amount and types of fatty acids acutely affect insulin, glycemic and gastrointestinal peptide responses but not satiety in metabolic syndrome subjects

Chang CY, Kanthimathi MS, Tan AT, Nesaretnam K, Teng KT

Eur J Nutr, 2018 Feb;57(1):179-190.
PMID: 27632019 DOI: 10.1007/s00394-016-1307-9

PURPOSE: Limited clinical evidence is available on the effects of amount and types of dietary fats on postprandial insulinemic and gastrointestinal peptide responses in metabolic syndrome subjects. We hypothesized that meals enriched with designated: (1) amount of fats (50 vs 20 g), (2) fats with differing fatty acid composition (saturated, SFA; monounsaturated, MUFA or n-6 polyunsaturated fatty acids, PUFA) would affect insulinemic and gastrointestinal peptide releases in metabolic syndrome subjects.
METHODS: Using a randomized, crossover and double-blinded design, 15 men and 15 women with metabolic syndrome consumed high-fat meals enriched with SFA, MUFA or n-6 PUFA, or a low-fat/high-sucrose (SUCR) meal. C-peptide, insulin, glucose, gastrointestinal peptides and satiety were measured up to 6 h.
RESULTS: As expected, SUCR meal induced higher C-peptide (45 %), insulin (45 %) and glucose (49 %) responses compared with high-fat meals regardless of types of fatty acids (P < 0.001). Interestingly, incremental area under the curve (AUC0-120min) for glucagon-like peptide-1 was higher after SUCR meal compared with MUFA (27 %) and n-6 PUFA meals (23 %) (P = 0.01). AUC0-120min for glucose-dependent insulinotropic polypeptide was higher after SFA meal compared with MUFA (23 %) and n-6 PUFA meals (20 %) (P = 0.004). Significant meal x time interaction (P = 0.007) was observed for ghrelin, but not cholecystokinin and satiety.
CONCLUSIONS: The amount of fat regardless of the types of fatty acids affects insulin and glycemic responses. Both the amount and types of fatty acids acutely affect the gastrointestinal peptide release in metabolic syndrome subjects, but not satiety.

Matched MeSH terms: Ghrelin/blood

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