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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sympathoexcitatory effects of insulin are well-established, although the exact mechanisms by which insulin stimulates the sympathetic nervous system are not completely understood. The majority of research supports a primary role for the central nervous system in the gradual and sustained rise in muscle sympathetic nerve activity (MSNA) in response to hyperinsulinemia; in addition, recent studies in animals suggests carotid body chemoreceptors respond to increases in systemic insulin levels. Intermittent activation of the carotid chemoreceptors, similar to that seen in patients with sleep apnea, can result in sensory long term facilitation and may contribute to the observed rise in baseline MSNA in this population. Consistent with this idea, insulin exposure results in sustained increases in MSNA that persist even when plasma insulin levels return to baseline. We propose the carotid chemoreceptors contribute to insulin-mediated sympathoexcitation and the persistent rise in MSNA in patients with sustained hyperinsulinemia. If the carotid chemoreceptors sense and respond to changes in systemic insulin levels, these organs may provide a viable target for the treatment of disorders known to exhibit sustained hyperinsulinemia and sympathoexcitation including, but not limited to, obesity, hypertension, sleep apnea, metabolic syndrome, cardiovascular disease, and diabetes.
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PMID:Is insulin the new intermittent hypoxia? 2469 Feb 99

Obesity, particularly severe obesity is capable of producing hemodynamic alterations that contribute to changes in cardiac morphology which may predispose to impairment of ventricular function and heart failure. These include a high cardiac output state in most, left ventricular (LV) hypertrophy, and LV diastolic dysfunction. Right heart involvement may result from LV failure, the hypercirculatory state, and sleep disordered breathing. In recent years experimental studies and some studies in humans suggest that certain neurohormonal and metabolic alterations that occur commonly in obesity may contribute to alterations in cardiac structure and function. These include activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, hyperleptinemia due to leptin resistance, low circulating adiponectin levels, insulin resistance with hyperinsulinemia, and possibly cardiac lipotoxicity. This review will describe the ways in which these factors weave together to promote adaptations and maladaptations that result in alterations in cardiac structure and function which may contribute to the development of heart failure.
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PMID:Obesity and Cardiac Remodeling in Adults: Mechanisms and Clinical Implications. 2999 May 33


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