Neuropeptide Y, leptin, galanin and insulin in women with polycystic ovary syndrome

Baranowska, B; Radzikowska, M.; Wasilewska-Dziubińska, Elżbieta; Kapliński, A; Roguski, Krzysztof; Płonowski, Artur

doi:10.3109/09513599909167578

Cited by 55 publications

(54 citation statements)

References 26 publications

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“…However in severely obese, polycystic ovarian syndrome (PCOS) patients it has been observed that this inverse relationship between leptin and NPY is lost. NPY levels are often elevated, yet some PCOS patients exhibit equal to or higher than expected leptin levels likely due to endocrine dysregulation [41][42][43] which is consistent with our observations in this study. Furthermore, NPY response to ghrelin is also defective in PCOS patients [41].…”

Section: Doi: 107243/2050-0866-2-23supporting

confidence: 91%

“…NPY levels are often elevated, yet some PCOS patients exhibit equal to or higher than expected leptin levels likely due to endocrine dysregulation [41][42][43] which is consistent with our observations in this study. Furthermore, NPY response to ghrelin is also defective in PCOS patients [41]. This evidence, taken together with our current study, suggests a general uncoupling of hormonal feedback mechanisms.…”

Section: Doi: 107243/2050-0866-2-23supporting

confidence: 91%

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Peripartum changes in the orexigenic CNS peptide neuropeptide-Y in gestational diabetics

Anchan

Lindsey²,

Newton³

et al. 2013

J Diab Res Clin Met

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Background: Development of relative insulin resistance during pregnancy is a normal physiologic change related to placental lactogen and pregnancy-associated elevated lipid concentrations. Several studies have investigated the role of tissue response, tyrosine kinase insulin receptor phosphorylation, and other cytokines that might contribute to development of such resistance. In this study, we specifically investigate the accompanying changes in concentrations of the orexigenic neurotransmitter neuropeptide Y (NPY) during pregnancy with the development and resolution of insulin resistance in gestational diabetics. Given that increased NPYergic activity is associated with increased eating behavior and body weight, we hypothesize levels of the central nervous system (CNS) peptide NPY will shift, along with other factors such as adiponectin, leptin, and ghrelin, in the development and resolution of gestational diabetes mellitus. Methods: Antepartum and postpartum plasma concentrations of NPY, leptin, ghrelin, tumor necrosis factor-alpha, glucose, and insulin were measured in gravid patients that were healthy (N=22), class A1 and A2 gestational diabetics (N=8), or type 2 diabetics (N=4). Homeostatic Model Assessment of insulin resistance was also calculated. Data was analyzed using a t-test and considered significant with p<0. 05. Results: We demonstrate that during the third trimester, class A2 gestational diabetics display an elevated NPY concentration. This elevated NPY begins to resolve immediately postpartum, normalizing by the patient's 6 week postpartum visit. The associated Homeostatic Model Assessment of insulin resistance index (HOMA) is consistent with these observations showing a concomitant elevation of HOMA intrapartum with improved insulin resistance within 24 hours postpartum. Discussion: Collectively, these results suggest a role for central nervous system involvement in the development of insulin resistance during gestational diabetes. Additionally, rising NPY levels during pregnancy may warrant routine patient surveillance for the development of occult insulin resistance and the obstetrical management of the same.

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Section: Doi: 107243/2050-0866-2-23supporting

confidence: 91%

Section: Doi: 107243/2050-0866-2-23supporting

confidence: 91%

Peripartum changes in the orexigenic CNS peptide neuropeptide-Y in gestational diabetics

Anchan

Lindsey²,

Newton³

et al. 2013

J Diab Res Clin Met

View full text Add to dashboard Cite

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“…In this context our recent data from a study comprising of 2 groups of overweight insulin-resistant PCOS women [150] showed that a 3-month treatment with metformin (Group 1) and rosiglitazone (Group 2), added to an oral hormone contraceptive (OHC) (a standard combination of ethynil oestradiol 35 g plus cyproterone acetate 2 mg) resulted in decrease of atherogenic adipocytokines (leptin, resistin, and TNF ) ( Table 2) that may have beneficial effects in the future prevention of atherosclerosis and cardiovascular diseases in this risk cohort of young women. But the serum concentrations of NPY also decreased that is in support of some our previous [151] and other authors [143,144] data for impaired NPYleptin link in PCOS. The change of NPY and adipocytokines was associated with weight loss only in the metformin group that is an expected effect of the drug and in conformity with other studies [150].…”

Section: Npy and Reproductive Functionsupporting

confidence: 91%

“…The increase in NPY in their study was independent of the increase in BMI. In obese women with PCOS, plasma leptin was increased compared to lean women [143]. Bidzińńska-Speichert et al [144] also found higher leptin and NPY levels and lower galanin levels in PCOS women as compared to healthy controls [144].…”

Section: Npy and Reproductive Functionmentioning

confidence: 92%

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Appetite Regulatory Peptides and Insulin Resistance

Orbetzova¹

2012

Insulin Resistance

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In addition to leptin and insulin, receptors for ghrelin are also located on arcuate AgRP/NPY neurons, which are activated by central ghrelin administration. Furthermore, peripheral ghrelin administration activates neurons in the ARC and AgRP and NPY have been demonstrated to be requisite mediators of the hyperphagia induced by systemic ghrelin [11]. So, meal-generated satiety signals from the GI tract do interact with longer-term adiposity signals, such as insulin and leptin in energy balance [8].NPY is one of the most abundant peptides of the hypothalamus and one of the most potent orexigenic factors. The majority of neurons expressing NPY in the hypothalamus are found within the ARC and most co-express AgRP [14]. Synthesis and release of NPY are both regulated by leptin binding to its hypothalamic receptor. NPY links afferents reflecting the nutritional status of the organism from endocrine, gastrointestinal, and central and peripheral nervous systems to effectors of energy intake and expenditure [15]. NPY stimulates appetite inducing hyperphagia, increase of fat depots, decrease of thermogenesis, and suppression of sympathetic activity. NPY is known to be involved in other physiological functions, such as cardiovascular regulation, affective disorder, memory retention, neuroendocrine control. When leptin levels increase after food intake, the latter binds to its receptors in the hypothalamus which leads to discontinuation of NPY secretion [5,16]. The decrease of NPY concentration in obesity probably plays a role of a counterregulatory factor intended to prevent further weight gain. Thus, NPY becomes one of the main regulators of food intake, body weight and energy expenditure.Ghrelin is a fast-acting hormone, seemingly playing a role in meal initiation. Secreted predominantly from the stomach, ghrelin is the natural ligand for the growth hormone secretagogue-receptor (GHS-R) in the pituitary gland, thus fulfilling the criteria of a brain- gut peptide [5,6]. Although the majority of ghrelin is produced peripherally, there are ghrelin immunoreactive neurons within the hypothalamus that have terminals on hypothalamic NPY/AgRP, POMC and corticotropin releasing hormone (CRH) neurons [17], as well as orexin fibres in the LHA [18]. It was found that ghrelin acts to promote appetite in two ways-directly, by depolarizing the orexigenic NPY/AgRP neurons, and indirectly, by increasing the tonic inhibition exerted by the NPY/AgRP neurons over the anorexigenic POMC/CART neurons. Both of these ultimately enhance appetite [4,17,18]. The ability of ghrelin to increase food intake and body weight is mediated through the stimulation of NPY production in the hypothalamic ARC, where it antagonizes the inhibitory effect on NPY secretion displayed by leptin and insulin [19].The purpose of this chapter is to provide background information on the relationship between the main appetite regulatory peptides NPY and ghrelin, and insulin resistance. The role of NPY and ghrelin in food intake and body weight control in humans, and their ...

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Maternal Diet, Oocyte Nutrition and Metabolism, and Offspring Health

Velazquez

Fleming

2012

Oogenesis

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Neuropeptide Y, leptin, galanin and insulin in women with polycystic ovary syndrome

Cited by 55 publications

References 26 publications

Peripartum changes in the orexigenic CNS peptide neuropeptide-Y in gestational diabetics

Peripartum changes in the orexigenic CNS peptide neuropeptide-Y in gestational diabetics

Appetite Regulatory Peptides and Insulin Resistance

Maternal Diet, Oocyte Nutrition and Metabolism, and Offspring Health

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