Neuropeptide Y Leu7Pro Polymorphism Associated With the Metabolic Syndrome and Its Features in Patients With Coronary Artery Disease

Masoudi-Kazemabad, Ali; Jamialahmadi, Khadijeh; Moohebati, Mohsen; Mojarrad, Majid; manshadi, R. Dehghan; Akhlaghi, Saeed; Ferns, Gordon A.; Ghayour‐Mobarhan, Majid

doi:10.1177/0003319711435149

Cited by 13 publications

(11 citation statements)

References 24 publications

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“…This single nucleotide polymorphism (SNP) has been associated with a large number of conditions related to obesity and metabolic syndrome traits, including increased BMI in adults (194), development of obesity in young adults (195), risk of hypertension (196), high plasma low-density lipoprotein-cholesterol (LDL-c) in children and adults (196, 197), and elevated plasma TAG (198). This variant has been associated with metabolic syndrome in patients with coronary artery disease (199). This SNP has also been shown to correlate with high birth body weight in preschoolers, the risk of an accelerated atherosclerotic process or carotid atherosclerosis in adults (196, 200), and the risk of type 2 diabetes mellitus in adults (201).…”

Section: Implications For Obesity and Metabolic Syndromementioning

confidence: 99%

Peptides and Food Intake

et al. 2014

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The mechanisms for controlling food intake involve mainly an interplay between gut, brain, and adipose tissue (AT), among the major organs. Parasympathetic, sympathetic, and other systems are required for communication between the brain satiety center, gut, and AT. These neuronal circuits include a variety of peptides and hormones, being ghrelin the only orexigenic molecule known, whereas the plethora of other factors are inhibitors of appetite, suggesting its physiological relevance in the regulation of food intake and energy homeostasis. Nutrients generated by food digestion have been proposed to activate G-protein-coupled receptors on the luminal side of enteroendocrine cells, e.g., the L-cells. This stimulates the release of gut hormones into the circulation such as glucagon-like peptide-1 (GLP-1), oxyntomodulin, pancreatic polypeptides, peptide tyrosine tyrosine, and cholecystokinin, which inhibit appetite. Ghrelin is a peptide secreted from the stomach and, in contrast to other gut hormones, plasma levels decrease after a meal and potently stimulate food intake. Other circulating factors such as insulin and leptin relay information regarding long-term energy stores. Both hormones circulate at proportional levels to body fat content, enter the CNS proportionally to their plasma levels, and reduce food intake. Circulating hormones can influence the activity of the arcuate nucleus (ARC) neurons of the hypothalamus, after passing across the median eminence. Circulating factors such as gut hormones may also influence the nucleus of the tractus solitarius (NTS) through the adjacent circumventricular organ. On the other hand, gastrointestinal vagal afferents converge in the NTS of the brainstem. Neural projections from the NTS, in turn, carry signals to the hypothalamus. The ARC acts as an integrative center, with two major subpopulations of neurons influencing appetite, one of them coexpressing neuropeptide Y and agouti-related protein (AgRP) that increases food intake, whereas the other subpopulation coexpresses pro-opiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript that inhibits food intake. AgRP antagonizes the effects of the POMC product, α-melanocyte-stimulating hormone (α-MSH). Both populations project to areas important in the regulation of food intake, including the hypothalamic paraventricular nucleus, which also receives important inputs from other hypothalamic nuclei.

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Section: Implications For Obesity and Metabolic Syndromementioning

confidence: 99%

Peptides and Food Intake

et al. 2014

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“…Based on the data from NHANES collected between 1999 and 2002, the prevalence of Met Syndrome is 34.5% (11,12). Also Azimi-Nejad et al found that the "prevalence of Met syndrome was higher in Iranian women (55.0%), followed by Iranian men (30.1%), and this was higher than in French men (13.7%) and French women (6.6%) (13).…”

Section: Contextmentioning

confidence: 99%

Ocular Manifestations of Metabolic Syndrome

Rahimi¹,

Omidtabrizi²,

Mobarhan³

et al. 2014

Razavi Int J Med

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Context: Metabolic syndrome (metabolic syndrome X) is a prevalent cluster of risk factors that include high BMI, hypertension, insulin resistance and dyslipidemia. Individuals with metabolic syndrome are at an increased risk of coronary artery disease (CAD) and diabetes mellitus. Diabetes mellitus and hypertension (HTN) are associated with retinopathy and cataract. Evidence Acquisition: Bibliographical searches were performed using MEDLINE/ScienceDirect/OVID up to October 2013 using the following keywords (all fields): ("metabolic syndrome" OR "Met syndrome") AND [(ocular disease) OR (cataract) OR (glaucoma) OR (agerelated maculopathy). Results: This review explores the relationship between metabolic syndrome, including all its components, and various ocular conditions such as retinopathy, central retinal artery occlusion, cataract and elevated intraocular pressure. Conclusions: Today, the prevalence of metabolic syndrome is increasing, because world population life in prevalence behaviors have changed. Its association with various ocular manifestations such as non-diabetic retinopathy, CRAO, cataract, and primary open angle glaucoma suggests that an epidemic of Met syndrome can have far-fetched ocular consequences as well.

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“…Based on these findings, the obesogenic role of peripheral Y 2 -receptors seems quite convincing and antagonism of peripheral Y 2 -receptors a plausible anti-obesity drug strategy. To this end, we aimed to test the anti-obesity effects of chronic treatment with a specific Y 2 -receptor antagonist with a potential clinical application to be obesity and metabolic disorders due to NPY excess induced by chronic stress or genetic factors (gain-of-function polymorphisms) ( Karvonen et al, 1998 ; Ding et al, 2005 ; Masoudi-Kazemabad et al, 2013 ). In order to study this, transgenic mice overexpressing NPY in noradrenergic neurons (OE-NPY DβH ) and wildtype (WT) control mice were subjected to chow or DIO with Western type diet and treated with peripheral Y 2 -receptor antagonist, BIIE0246, which is highly selective for its receptors ( Doods et al, 1999 ) and unable to penetrate the blood-brain barrier ( Brothers et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Peripherally Administered Y2-Receptor Antagonist BIIE0246 Prevents Diet-Induced Obesity in Mice With Excess Neuropeptide Y, but Enhances Obesity in Control Mice

et al. 2018

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Neuropeptide Y (NPY) plays an important role in the regulation of energy homeostasis in the level of central and sympathetic nervous systems (SNSs). Genetic silencing of peripheral Y2-receptors have anti-obesity effects, but it is not known whether pharmacological blocking of peripheral Y2-receptors would similarly benefit energy homeostasis. The effects of a peripherally administered Y2-receptor antagonist were studied in healthy and energy-rich conditions with or without excess NPY. Genetically obese mice overexpressing NPY in brain noradrenergic nerves and SNS (OE-NPYDβH) represented the situation of elevated NPY levels, while wildtype (WT) mice represented the normal NPY levels. Specific Y2-receptor antagonist, BIIE0246, was administered (1.3 mg/kg/day, i.p.) for 2 or 4.5 weeks to OE-NPYDβH and WT mice feeding on chow or Western diet. Treatment with Y2-receptor antagonist increased body weight gain in both genotypes on chow diet and caused metabolic disturbances (e.g., hyperinsulinemia and hypercholesterolemia), especially in WT mice. During energy surplus (i.e., on Western diet), blocking of Y2-receptors induced obesity in WT mice, whereas OE-NPYDβH mice showed reduced fat mass gain, hepatic glycogen and serum cholesterol levels relative to body adiposity. Thus, it can be concluded that with normal NPY levels, peripheral Y2-receptor antagonist has no potential for treating obesity, but oppositely may even induce metabolic disorders. However, when energy-rich diet is combined with elevated NPY levels, e.g., stress combined with an unhealthy diet, Y2-receptor antagonism has beneficial effects on metabolic status.

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Neuropeptide Y Leu7Pro Polymorphism Associated With the Metabolic Syndrome and Its Features in Patients With Coronary Artery Disease

Cited by 13 publications

References 24 publications

Peptides and Food Intake

Peptides and Food Intake

Ocular Manifestations of Metabolic Syndrome

Peripherally Administered Y2-Receptor Antagonist BIIE0246 Prevents Diet-Induced Obesity in Mice With Excess Neuropeptide Y, but Enhances Obesity in Control Mice

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