Differential effects of insulin on sympathetic nerve activity in agouti obese mice
Open accessAbstract
OBJECTIVE: Hyperinsulinemia, which often coexists with obesity and type 2 diabetes, is a major risk factor for cardiovascular disease and thought to promote hypertension through the sympathetic effects of insulin. Here, we examined the effect of insulin on regional sympathetic nerve activity (SNA) in obesity. METHODS: Glucose and insulin tolerance tests were performed to examine insulin sensitivity in agouti obese mice. We used also multifiber recording to compare the regional SNA response to intracerebroventricular (ICV) insulin between lean and agouti obese mice. RESULTS: Agouti obese mice have significantly elevated levels of blood glucose and plasma insulin associated with glucose intolerance and insulin resistance. In lean mice, ICV administration of insulin (20 and 100 microU) caused a dose-dependent increase in SNA subserving hindlimb, kidney and brown adipose tissue (BAT). Of note, the regional SNA responses to insulin were differentially altered in agouti obese mice. Whereas lumbar SNA response to insulin was intact in the obese mice, renal and BAT sympathetic activation to insulin were significantly attenuated in these agouti obese mice. Finally, we assessed the role of phosphoinositol-3 kinase (PI3K) signaling pathway in mediating sympathetic activation to insulin in obesity. Notably, ICV pretreatment with a PI3K inhibitor (LY294002) blocked the increase in lumbar SNA induced by ICV insulin in lean and agouti obese mice. CONCLUSIONS: Our data suggest a differential regulation by insulin of sympathetic outflow to peripheral tissues in obesity. Our findings also demonstrate the importance of PI3K in lumbar sympathetic activation to insulin in obesity.
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The PI3K-MC4R axis mediates the preserved renal and lumbar sympathoexcitatory effects of leptin and insulin, respectively.
“Indeed, the PI3K-MC4R axis mediates the preserved renal and lumbar sympathoexcitatory effects of leptin (52;53) and insulin (51), respectively.”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [51]
Central action of insulin increases lumbar, but not renal, sympathetic nerve traffic in obese mice.
“Such possibility is consistent with the preserved ability of central action of insulin to increase lumbar, but not renal, sympathetic nerve traffic in obese mice (51).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [51]
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- Authors
- Morgan, D. A., & Rahmouni, K.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Rahmouni, Kamal
- Venue
- Journal of Hypertension
- Published
- 2010-09
- Volume
- 28
- Issue
- 9
- Pages
- 1913-1919
- ISSN
- 0263-6352 (ISSN-L)
- PMC
- PMC2920344
- OpenAlex
- W2120860188
- Cited by
- 46
- References
- 32
- Citations by year
- 2026: 2 · 2024: 8 · 2023: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2017: 5 · 2016: 2 · 2015: 4 · 2014: 7 · 2013: 4 · 2012: 2
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-084207, P01HL084207)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- insulin, sympathetic activity, obesity, insulin resistance, hyperinsulinemia, phosphoinositide 3-kinase signaling, renal sympathetic nerve activity, brown adipose tissue, hypertension
- MeSH terms
- Phosphoinositide-3 Kinase Inhibitors, Animals, Blood Glucose, Chromones, Disease Models, Animal, Enzyme Inhibitors, Injections, Intraventricular, Insulin, Insulin Resistance, Lumbosacral Region, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Morpholines, Obesity, Sympathetic Nervous System, Signal Transduction, Phosphatidylinositol 3-Kinases, Mice
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