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Cited by 21Regulation of Appetite and ObesityHypothalamic control of reproductive hormonesPharmacology and Obesity Treatment

Reduced ventromedial hypothalamic neuronal nitric oxide synthase and increased sensitivity to NOS inhibition in dietary obese rats: further evidence of a role for nitric oxide in the regulation of energy balance

Sadler, C.J, Wilding, J.P.H·2004·Brain Research
DOI 10.1016/j.brainres.2004.05.007
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Abstract

Inhibition of hypothalamic nitric oxide (NO) decreases energy intake, and changes in hypothalamic NO synthase (NOS) have been observed in genetically obese rodents, but it is not known if NO is involved in the development of diet-induced obesity (DIO). We therefore measured changes in hypothalamic neuronal NOS (nNOS) in DIO and investigated effects of peripheral and central inhibition of NOS in this model. Expression of nNOS in relation to changes in nutritional state was measured by immunohistochemistry, with radiochemical detection. The effect of chronic intraperitoneal (i.p.) administration of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day) on energy intake, bodyweight and hypothalamic nitric oxide content was assessed in both chow-fed and DIO animals. Twenty-four hour energy intake after acute intracerebroventricular (i.c.v.) of L-NAME was also measured. Diet-induced obese animals had a statistically significant 32% reduction in the number of nNOS-immunolabelled cells in the ventromedial hypothalamus compared to chow-fed controls. Intraperitoneal administration of L-NAME decreased hypothalamic NO content in both chow-fed and DIO. Energy intake was reduced by 16% in DIO over 16 days, whereas energy intake was only reduced by 11% in chow-fed animals, although both were statistically significant. L-NAME significantly reduced body weight gain in DIO but not in chow-fed rats. L-NAME administered i.c.v. decreased 24 h energy intake to a greater extent in DIO rats, by 18%, compared with a 10% reduction in chow-fed rats. Ventromedial hypothalamic expression of nNOS is sensitive to changes in nutritional state. Despite having reduced nNOS, dietary obese rats were more sensitive to the effects of NOS inhibition than lean controls, suggesting a role for NO in the development of hyperphagia and obesity in rats fed a palatable diet.

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  • In rodents, L-arginine increases food intake and NOS inhibitors decrease food intake.

    “In rodents, L-arginine was shown to increase, and NOS inhibitors to decrease, food intake [155, 251-254].”

    From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [155]

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Authors
Sadler, C. J., & Wilding, J. P. H.
Affiliations
University of Liverpool (GB)
Corresponding author
Wilding, J.P.H
ORCID
Wilding, J.P.H
Venue
Brain Research
Publisher
Elsevier BV
Published
2004-08
Volume
1016
Issue
2
Pages
222-228
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2004.05.007
OpenAlex
W2082825849
Cited by
21
References
28
Citations by year
2023: 1 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 1 · 2012: 3
FWCI
0.35
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
  • Health Sciences › Medicine › Pharmacology › Pharmacology and Obesity Treatment
Keywords
nitric oxide, neuronal nitric oxide synthase, ventromedial hypothalamus, diet-induced obesity, energy balance, energy intake, L-NAME, nitric oxide synthase inhibition, hyperphagia, weight gain, palatable diet, nutritional status
MeSH terms
Analysis of Variance, Animals, Body Weight, Energy Intake, Cell Count, Diet, Enzyme Inhibitors, Immunohistochemistry, Male, Nitric Oxide, Obesity, Ventromedial Hypothalamic Nucleus, Rats, Wistar, Nitric Oxide Synthase, NG-Nitroarginine Methyl Ester, Rats, Nitric Oxide Synthase Type I

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