PI3K signaling: A key pathway in the control of sympathetic traffic and arterial pressure by leptin

Harlan, Shannon M.; Rahmouni, Kamal

doi:10.1016/j.molmet.2013.03.004

Cited by 23 publications

(26 citation statements)

References 58 publications

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“…The autonomic nervous system (ANS) innervates and regulates metabolic organs and plays an important role in physiological responses to endogenous and exogenous stimuli. The ANS consists of two parts, the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) [13][14][15][16]. Traditionally, the SNS has been associated with catabolic responses and the PSNS with anabolic responses [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

“…The ANS consists of two parts, the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) [13][14][15][16]. Traditionally, the SNS has been associated with catabolic responses and the PSNS with anabolic responses [14][15][16][17]. Under some physiological circumstances, both the SNS and PSNS can be activated or inhibited at the same time, but usually when one is activated the other is inhibited [18].…”

Section: Introductionmentioning

confidence: 99%

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Hypothalamic-autonomic control of energy homeostasis

et al. 2015

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Regulation of energy homeostasis is tightly controlled by the central nervous system (CNS). Several key areas such as the hypothalamus and brainstem receive and integrate signals conveying energy status from the periphery, such as leptin, thyroid hormones, and insulin, ultimately leading to modulation of food intake, energy expenditure (EE), and peripheral metabolism. The autonomic nervous system (ANS) plays a key role in the response to such signals, innervating peripheral metabolic tissues, including brown and white adipose tissue (BAT and WAT), liver, pancreas, and skeletal muscle. The ANS consists of two parts, the sympathetic and parasympathetic nervous systems (SNS and PSNS). The SNS regulates BAT thermogenesis and EE, controlled by central areas such as the preoptic area (POA) and the ventromedial, dorsomedial, and arcuate hypothalamic nuclei (VMH, DMH, and ARC). The SNS also regulates lipid metabolism in WAT, controlled by the lateral hypothalamic area (LHA), VMH, and ARC. Control of hepatic glucose production and pancreatic insulin secretion also involves the LHA, VMH, and ARC as well as the dorsal vagal complex (DVC), via splanchnic sympathetic and the vagal parasympathetic nerves. Muscle glucose uptake is also controlled by the SNS via hypothalamic nuclei such as the VMH. There is recent evidence of novel pathways connecting the CNS and ANS. These include the hypothalamic AMP-activated protein kinase-SNS-BAT axis which has been demonstrated to be a key modulator of thermogenesis. In this review, we summarize current knowledge of the role of the ANS in the modulation of energy balance.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hypothalamic-autonomic control of energy homeostasis

et al. 2015

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“…Besides its interaction with the PIK/AKT pathway, possibly implicated in early cytodegenerative processes of myelin, the actions of Leptin include a strong influence in both the innate and the adaptive immune system. In the innate system, Leptin stimulate the activation of the monocyte-macrophage lineage and the secretion of pro-inflammatory cytokines; in the adaptive immune system Leptin induces proinflammatory Th1 responses [61,62]. Interestingly, the Leptin deficient mice are resistant to the induction of EAE, and administration of Leptin in this animal model shifts the Th2-type response, characteristic of this animal model, to a Th1-type response [68].…”

Section: Obesity and Leptin: Correlations Between Metabolism And Paedmentioning

confidence: 83%

“…A number of studies have demonstrated the relevance of PI3K as an underlying mechanism of Leptin actions in vivo [52]. In rats, peripheral Leptin administration was found to activate PI3K in the brain and pre-treatment with inhibitors of PI3K abolished the anorectic response induced by Leptin [61][62][63].…”

Section: Obesity and Leptin: Correlations Between Metabolism And Paedmentioning

confidence: 99%

The role of puberty and adolescence in the pathobiology of pediatric multiple sclerosis

Salpietro

Polizzi

Recca

et al. 2018

Mult Scler Demyelinating Disord

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Multiple sclerosis (MS) is increasingly recognized in the paediatric age. In a smaller, but well-established, proportion of paediatric MS patients [20% of total paediatric MS cases: 0.2% to 0.7% of the total MS patients] the onset of disease is before 10 years of age [pre-pubescent (childhood) MS]; in the majority [80%] of paediatric MS patients, however [1.7% to 5.6% of the total MS population], the onset of disease is between 10 and 18 years [post-pubertal (juvenile) MS]. Notably, while pre-pubertal MS occurs almost equally in both genders (female/male ratio = 0.9:1; reverting to 0.4-0.6/1 in pre-school MS children) the female/male ratio rises to 2.2/3:1 in the post-pubertal age. Interestingly, precocious puberty has been associated to: (a) a higher risk of developing MS; and (b) a more severe disease course. In addition to that, males are more susceptible to MS (and manifest more neurodegeneration) than females the latter being however more inflammatory than males; pregnancy however reduces MS relapses. All the above findings led to the suggestion of an underlying female sex hormonal involvement in the pathophysiology of MS vs. a protective role of male sex hormones. Epigenetic perspectives indicate that the interplay between genetic background, environmental triggers and neuroendocrine changes, typically occurring around the time of adolescence, could all play a combined role in initiating and/or promoting MS with onset in the paediatric age including many of the most frequent disease-associated risk factors (e.g., overweight/obesity, low vitamin D levels, reduced sunlight exposure, Epstein-Barr virus infection). According to this proposed complex multifactorial model, susceptibility to MS may be thus acquired during pre-pubertal age and children have probably to wait until the adolescence to manifest their first clinical signs/symptoms.

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“…In obese animals and patients, although resistance to the anorexigenic action of leptin has been clearly documented, leptin's sympathetic effects are preserved [ 44 ]. Thus, despite failing to regulate food intake and body weight, leptin appears to have a signifi cant role in the development of hypertension in obesity [ 42 ].…”

Section: Hyperleptinemiamentioning

confidence: 99%

Sympathetic and Renin–Angiotensin Activity in the Pathophysiology of Hypertension

Covic

Segall

2015

Pathophysiology and Pharmacotherapy of Cardiovascular Disease

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The implication of the sympathetic nervous system (SNS) in the pathogenesis of essential hypertension has been suggested a long time ago, considering the major role played by this system in blood pressure (BP) regulation. Studies based on both global (e.g., plasma norepinephrine) and regional (norepinephrine spillover and microneurography) assessments of sympathetic activity have demonstrated that neurogenic mechanisms may be involved in up to 50 % of all cases of essential hypertension. In addition, renal sympathetic denervation has been shown to induce signifi cant and persistent decreases in BP. Moreover, there is evidence that sympathetic hyperactivity may contribute directly to target-organ damage, including cardiac hypertrophy, vascular remodeling, and renal dysfunction. The specifi c causes of sympathetic activation in essential hypertension are not entirely known, but genetic factors, high dietary salt intake, as well as several metabolic and neurohumoral abnormalities have been involved. In patients with obesity-and metabolic syndrome-associated hypertension, SNS overactivity may result from many factors, including hyperinsulinemia, hyperleptinemia, hypoadiponectinemia, hypoghrelinemia, and RAAS activation.The renin-angiotensin system (RAS) is another key regulator of BP and fl uid homeostasis. Ang II induces BP elevation by vasoconstriction of renal and systemic arterioles, stimulation of renal tubular sodium reabsorption, and release of aldosterone from the adrenal glands. Moreover, both Ang II (via AT 1 receptors) and aldosterone exert proinfl ammatory, profi brotic, and prooxidant effects on the cardiovascular system, contributing to myocardial hypertrophy and fi brosis, vascular remodeling and calcifi cation, cerebrovascular damage, and renal glomerular and tubulointerstitial injury. In contrast, other components of the RAS, including mainly the AT 2 receptors and the ACE2/Ang-(1-7)/Mas axis, counteract most of the negative cardiovascular effects of the Ang II/AT 1 /aldosterone system and might play a compensatory role in hypertension.

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PI3K signaling: A key pathway in the control of sympathetic traffic and arterial pressure by leptin

Cited by 23 publications

References 58 publications

Hypothalamic-autonomic control of energy homeostasis

Hypothalamic-autonomic control of energy homeostasis

The role of puberty and adolescence in the pathobiology of pediatric multiple sclerosis

Sympathetic and Renin–Angiotensin Activity in the Pathophysiology of Hypertension

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