Relation of leptin and insulin to adiposity-associated elevations in sympathetic activity with age in humans

Monroe, Mary Beth Browning; Pelt, Rachael E. Van; Schiller, Brian C.; Seals, Douglas R.; Jones, P. P.

doi:10.1038/sj.ijo.0801364

Cited by 62 publications

(54 citation statements)

References 38 publications

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“…Some of these findings for baseline ASF constitute replications and strongly warrant follow-up work to identify the genes and mutations responsible for fat accumulation in the abdominal depot. Results for baseline AVF (i.e., promising linkage with IRS1 and suggestive results for the leptin gene) are biologically consistent with reported phenotypic associations among abdominal visceral adiposity, insulin sensitivity, and leptin concentrations (49,50); replication of this result in an independent study is needed. …”

Section: Discussionsupporting

confidence: 57%

A Genomewide Linkage Scan for Abdominal Subcutaneous and Visceral Fat in Black and White Families

et al. 2002

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Abdominal visceral fat (AVF), abdominal subcutaneous fat (ASF), and abdominal total fat (ATF) were measured using a computed tomography scan, both before (baseline) and after (post) a 20-week endurance exercise training protocol in the HERITAGE Family Study. Each of the baseline and response (post minus baseline) measures was adjusted for several covariates, including total fat mass, and responses to training were further adjusted for baseline levels. Multipoint variance components linkage analysis using a genomewide scan of 344 markers was conducted separately by race using race-specific allele frequencies. Several promising results (P < 0.0023) were obtained. For baseline AVF, the best evidence was on 2q22.1 and 2q33.2-q36.3 (including the IRS1 locus) in whites, with suggestive findings on 7q22.2-q31.3 (including the LEP locus) in blacks. Although several regions were indicated for baseline ASF, only 4q31.22-q32.2 and 11p15.4-p11.2 replicated the results of another study. For responses to training, promising results were limited to ASF and ATF primarily on 7q36.2 (including NOS3) in blacks, with suggestive regions (P < 0.01) on 1q21.2-q24.1 (S100A, ATP1A2, and ATP1B1), 10q25.2 (ADRA2A), and 11p15.5 (IGF2). In summary, the 4q and 11p regions have now been implicated in two independent studies for ASF; further research is warranted to identify the genes and mutations in these regions that are responsible for fat accumulation in the abdominal depot. Additional work in an independent sample is needed to verify the linkages for baseline AVF as well as the response measures.

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Section: Discussionsupporting

confidence: 57%

A Genomewide Linkage Scan for Abdominal Subcutaneous and Visceral Fat in Black and White Families

et al. 2002

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“…However, whether hyperleptinemia could be a potential mechanism contributing to SNS activation (and BP) elevations in obese humans is unclear. Leptin concentrations have been inconsistently related to MSNA (Snitker et al, 1997, Monroe et al, 2000. In addition, expression and secretion of leptin is lower in visceral compared with subcutaneous adipocytes (Russell et al, 1998) and circulating concentrations of the protein are similar in humans with higher compared with lower abdominal visceral fat but similar total and subcutaneous abdominal fat (unpublished observations).…”

Section: Potential Mechanisms Of Sympathetic Nervous System Activatiomentioning

confidence: 95%

“…However, several lines of evidence suggest otherwise. First, fasting insulin concentrations have been related to MSNA in some (Scherrer et al, 1994, Monroe et al, 2000, Weyer et al, 2000 but not all studies . Second, intranasal delivery of insulin, which does not accumulate systemically, appears not to increase MSNA (Benedict et al, 2005).…”

Section: Potential Mechanisms Of Sympathetic Nervous System Activatiomentioning

confidence: 99%

Sympathetic nervous system behavior in human obesity

Davy

Orr

2009

Neuroscience & Biobehavioral Reviews

143

121

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The sympathetic nervous system (SNS) plays an essential role in the regulation of metabolic and cardiovascular homeostasis. Low SNS activity has been suggested to be a risk factor for weight gain and obesity development. In contrast, SNS activation is characteristic of a number of metabolic and cardiovascular diseases that occur more frequently in obese individuals. Until recently, the relation between obesity and SNS behavior has been controversial because previous approaches for assessing SNS activity in humans have produced inconsistent findings. Beginning in the early 1990's, many studies using state of the art neurochemical and neurophysiological techniques have provided important insight. The purpose of the present review is to provide an overview of our current understanding of the regional specific alterations in SNS behavior in human obesity. We will discuss findings from our own laboratory which implicate visceral fat as an important depot linking obesity with skeletal muscle SNS activation. The influence of weight change on SNS behavior and the potential mechanisms and consequences of region specific SNS activation in obesity will also be considered.

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“…Although both insulin and leptin may activate the sympathetic nervous system, regional patterns of sympathetic activation differ with these peptides. Additionally, in humans, the multivariate analysis shows that MSNA seems to be more related to plasma leptin than to insulin 67 .…”

Section: Potential Mechanisms That May Contribute To Sympathetic Actimentioning

confidence: 99%

Desequilíbrio autonômico e síndrome metabólica: parceiros patológicos em uma pandemia global emergente

Lopes¹,

Egan²

2006

Arq. Bras. Cardiol.

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This review will examine the importance of the autonomic nervous system both in the pathophysiology and complications of the metabolic syndrome. Metabolic syndrome refers to a constellation of risk factors related to insuline resistance and obesity with a pattern of central fat distribution. While the insulin resistance syndrome has been attracting attention over the last three decades, the metabolic syndrome achieved heightened prominence after the publication and review of the World Health Organization (WHO) Expert Committee Report on the diagnosis and classification of diabetes mellitus, in 1998, and the National Cholesterol Education Program guidelines (Adult Treatment Panel [ATP] III) in 2001, in the United states [1][2][3] . Although definitions provided differ somewhat, both anticipate a significant increase in the risk of coronary heart disease and cardiovascular disease in general [4][5][6] .The metabolic syndrome affects a substantial proportion of adults in societies characterized by excessive calorie intake, use of labor-saving devices, and passive leisure activities. This syndrome is liable to become a pandemic, because obesity has been growing dramatically as the world's population ages 7 . Its costs, both in health and financial terms, are extremely high and can be more devastating than the largest armed conflict.This review focuses primarily on the role of the sympathetic nervous system in the metabolic syndrome, providing a gamut of information and directing its efforts rationally to prevent and treat the health consequences of this increasingly prevalent condition effectivelly. Metabolic syndrome DefinitionThe WHO and ATP-III definitions of the metabolic syndrome are not similar1-3 (Tab. 1). Associated risk factorsThis syndrome is associated with postprandial hyperinsulinemia, insulin resistance with reduced glucose and fatty acids, higher levels of denser LDL-cholesterol particles

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Relation of leptin and insulin to adiposity-associated elevations in sympathetic activity with age in humans

Cited by 62 publications

References 38 publications

A Genomewide Linkage Scan for Abdominal Subcutaneous and Visceral Fat in Black and White Families

A Genomewide Linkage Scan for Abdominal Subcutaneous and Visceral Fat in Black and White Families

Sympathetic nervous system behavior in human obesity

Desequilíbrio autonômico e síndrome metabólica: parceiros patológicos em uma pandemia global emergente

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