Intracerebroventricular Neuropeptide Y Acutely Influences Glucose Metabolism and Insulin Sensitivity in the Rat
Abstract
Acute administration of neuropeptide Y(NPY) into the hypothalamus and third cerebral ventricle (ICV) increases respiratory quotient, reduces energy expenditure and increases circulating, insulin, glucagon and corticosterone. Therefore, it is likely that hypothalamic NPY has acute effects on the metabolism of fuels, such as glucose. To test this hypothesis, we determined if ICV infusion of NPY influences glucose metabolism and its sensitivity to insulin in conscious, unrestrained rats, not given access to food. Glucose turnover was 4.7±0.3 mg/min, 45–55 min after ICV NPY was administered at 3 μg/h vs 3.7±0.2 (P<0.05) for ICV saline. In a time course study, glucose turnover was significantly increased 30 min, and remained elevated at 50 min after starting a similar ICV NPY infusion. In neither study was plasma glucose, insulin, glucagon or corticosterone significantly affected by ICV NPY. During an hyperinsulinaemic euglycaemic clamp, the glucose infusion rate corrected for body weight and insulin concentration, M/I was 0.22±0.03 for NPY vs 0.36±0.05 mg min−1 kg−1 μU−1 ml (P<0.05) for saline. NPY treatment prevented the decline in glucose production rate but did not influence the rise in glucose disposal rate resulting from hyperinsulinaemia. It was concluded that ICV NPY rapidly stimulates glucose turnover by a mechanism that does not depend on changes in insulin, glucagon or corticosterone secretion. Furthermore, ICV NPY decreased insulin sensitivity by reducing the effect of insulin on glucose production but not on whole body glucose disposal.
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Central administration of NPY and the melanocortin-3/4 receptor antagonist SHU9119 causes insulin resistance and glucose intolerance via mechanisms independent of food intake.
“Central administration of both NPY and the melanocortin-3/4 receptor antagonist, SHU9119, cause insulin resistance and glucose intolerance via mechanisms independent of their effects on food intake (1, 109, 188).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [109]
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“Central administration of both NPY and the melanocortin-3/4 receptor antagonist SHU9119 causes insulin resistance and glucose intolerance via mechanisms independent of their effects on food intake (1, 109, 188).”
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“ARH NPY acts centrally to regulate circulating insulin, glucagon, and corticosterone levels [Marks and Waite; 1997; Parikh and Marks, 1997] and to modulate insulin control of hepatic glucose production [van den Hoek et al., 2004].”
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Bisschop, P. H. L. T., Fliers, E., & Kalsbeek, A. (2015) · Comprehensive physiology · doi:10.1002/j.2040-4603.2015.tb00600.x · Cited by 7 · see citing works
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“neuropeptide Y (NPY), orexin-A (ORX), and oxytocin (OT) exert effects on blood glucose levels upon intracerebral administration (Bjorkstrand et al., 1996; Marks and Waite, 1997; Parikh and Marks, 1997; Sakurai et al., 1998; Yi et al., 2009), findings that support their potential function in vivo in neural pathways tha…”
BackgroundRestoring neuropetide Y levels in the hypothalamus ameliorates premature aging phenotype in mice
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“glucagon and corticosterone (Marke and Waite, 1997; Parikh and Marks, 1997) to hypoglycemia, the present evidence for acclimated transcriptional reactivity to RIIH raises the issue of possible NPY involvement in RIIH-associated counter-regulatory dysfunction.”
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AgRP1 modulates breeding season-dependent feeding behavior in female medakaPreprint
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“Like in mammals ( Marks et al., 1992 ; Clark et al., 1984 ; Glenn Stanley et al., 1986 ; Marks and Waite, 1997 ; Baldock et al., 2009 ), food restriction in zebrafish increased the npya expression in the hypothalamus ( Song et al., 2003 ; Opazo et al., 2018 ), and intracerebroventricular…”
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“…linked to carbohydrate homeostasis include GABA, NPY and or its insect functional homologue short neuropeptide F (sNPF), etc. (Grayson et al, 2013; Marks and Waite, 1997; Meng et al, 2016; Oh et al, 2019) Together, the modulation of carbohydrate homeostasis is comparatively conserved between…”
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AgRP1 modulates breeding season-dependent feeding behavior in female medaka
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LEPTIN— MUC HMOR ETHA N ASATIET YSIGNAL
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- Authors
- Marks, J. L., & Waite, K.
- Affiliations
- Westmead Hospital (AU)
- Corresponding author
- Marks, Jonathan L.
- ORCID
- Marks, Jonathan L.
- Venue
- Journal of Neuroendocrinology
- Publisher
- Wiley
- Published
- 1997-02
- Volume
- 9
- Issue
- 2
- Pages
- 99-103
- ISSN
- 0953-8194 (ISSN-L)
- 1365-2826
- OpenAlex
- W2028115360
- Cited by
- 80
- References
- 0
- Citations by year
- 2025: 5 · 2024: 2 · 2023: 2 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 7 · 2012: 4
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- neuropeptide Y, intracerebroventricular administration, glucose turnover, insulin sensitivity, glucose production, glucose disposal, hyperinsulinemic-euglycemic clamp, hypothalamus, energy metabolism, insulin resistance
- MeSH terms
- Animals, Blood Glucose, Corticosterone, Glucagon, Injections, Intraventricular, Insulin, Kinetics, Male, Neuropeptide Y, Glucose Clamp Technique, Rats, Wistar, Rats
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