title: [Defective nitric oxide homeostasis. Common underlying mechanism between insulin resistance, sympathetic overactivity and cardiovascular morbidity and mortality].
abstract: Obesity, insulin resistance and associated cardiovascular complications are reaching epidemic proportions worldwide and represent a major public health problem. Over the past decade, evidence has accumulated indicating that insulin administration, in addition to its metabolic effects, also has important cardiovascular actions. The sympathetic nervous system and the L-arginine-nitric oxide pathway are the central players in the mediation of insulin's cardiovascular actions. Based on recent animal and human research, we demonstrate that both defective and augmented NO synthesis represent a central defect triggering many of the metabolic, vascular and sympathetic abnormalities characteristic of insulin-resistant states. These observations provide the rationale for the use of pharmaceutical drugs releasing small and physiological amounts of NO and/or inhibitors of NO overproduction as a future treatment for insulin resistance and associated comorbidities.
authors.affiliation: Département de Médecine Interne, Centre Hospitalier Universitaire Vaudois, Lausanne, Suisse.
authors.forename: Marcos
authors.initials: M
authors.lastname: Schwab
authors.forename: Jonathan
authors.initials: J
authors.lastname: Bloch
authors.forename: Hervé
authors.initials: H
authors.lastname: Duplain
authors.forename: Claudio
authors.initials: C
authors.lastname: Sartori
authors.forename: Urs
authors.initials: U
authors.lastname: Scherrer
mesh_terms: D000818:Animals; D001682:Biological Availability; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D007333:Insulin Resistance / Q000502:physiology*; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000172:deficiency / Q000494:pharmacology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D051381:Rats; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D020030:Nitric Oxide Donors; D009569:Nitric Oxide; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III