2014
DOI: 10.4239/wjd.v5.i5.606
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Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Abstract: A re-examination of the mechanism controlling eating, locomotion, and metabolism prompts formulation of a new explanatory model containing five features: a coordinating joint role of the (1) autonomic nervous system (ANS); (2) the suprachiasmatic (SCN) master clock in counterbalancing parasympathetic digestive and absorptive functions and feeding with sympathetic locomotor and thermogenic energy expenditure within a circadian framework; (3) interaction of the ANS/SCN command with brain substrates of reward enc… Show more

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Cited by 32 publications
(24 citation statements)
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References 332 publications
(444 reference statements)
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“…15 Another cause of inflammation is oxidative stress, which can be triggered by adipocytes. When fat mass increases, insufficient irrigation can lead to lack of oxygen and, thus, to cell necrosis.…”
Section: Metabolic Syndrome and Oxidative Stressmentioning
confidence: 99%
“…15 Another cause of inflammation is oxidative stress, which can be triggered by adipocytes. When fat mass increases, insufficient irrigation can lead to lack of oxygen and, thus, to cell necrosis.…”
Section: Metabolic Syndrome and Oxidative Stressmentioning
confidence: 99%
“…Pathways involving the activation of melanocortin 4 receptors (MC4) is a key common mechanism mediating the increases in renal sympathetic nerve activity (RSNA) induced by leptin and insulin (Rahmouni et al, 2003), suggesting the potential for an interaction on RSNA, such that increased levels of both hormones could result in an additive action on RSNA. Interestingly both insulin and leptin can regulate each other's production and release, such that an increase in plasma levels of insulin can lead to an increase in leptin levels and vice versa (Santos et al, 2000; Borer, 2014), which further suggests potential interactions of the two hormones. Thus, in order to explore the possibility that insulin and leptin interact within the brain to induce greater increases in RSNA, the first aim of the present study was to compare RSNA in response to administration of leptin and insulin alone and in combination.…”
Section: Introductionmentioning
confidence: 99%
“…Insulin stimulates leptin release during meal-eating, and leptin then restrains all four of the insulin's actions as well as insulin release. It indirectly counter-regulates the energy storage actions of insulin by promoting lipolysis and stimulation of lipid metabolism (Borer, 2014). This endocrine counter-regulation of short-term energy balance is disrupted in obesity by the resistance of peripheral tissues to the actions of both insulin and leptin.…”
Section: The Endocrine Basis Of Obesity-associated Morbiditiesmentioning
confidence: 99%