Obesity Essay

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Obesity prevalence over the last three decades has risen markedly and is now affecting approximately 40% of the human population worldwide [1], an incidence that is starkly similar to that of heart disease, stroke and hypertension [2]. Although the main culprit for body fat deposition is the energy surplus, a growing body of evidence points to the apparent role of dietary, or added sugars, in this milieu. It is estimated that approximately 20% of regular western diet consists of added sugars, mainly as mixtures of glucose and fructose [3]. Whether the actions of glucose and fructose differ in terms of their effects on cardiovascular health and renal function remains unclear, although fructose has been suspected to play a pivotal role in…show more content…
In fact, it has recently been reported that moderate fructose intake in rats results in salt-sensitive hypertension that was associated with reduced cumulative sodium excretion and net positive sodium retention [12]. It is thus plausible that sodium and water retention are consequences of increased renal sympathetic nerve output. It is known that activation of the afferent renal sympathetic fibers in response to injury (i.e. heightened efferent SNS activity) initiates a renorenal reflex (negative feedback) with an overall goal to decrease efferent renal SNS output so as to facilitate renal sodium excretion[13]. It is also known that the renorenal reflex is impaired in spontaneously hypertensive rats resulting from increased activation of alpha2 adrenoreceptors and angiotensin II-type 1 receptors [14]. The status of the renorenal reflex in the fructose-fed rats has not been investigated.
The renal sympathetic nerves innervate the three major neuroeffectors in the kidney: juxtaglomerular granular cells, tubular epithelial cells and renal vasculature. Consequently, increased renal sympathetic nerve activity (RSNA) leads to increased renin secretion rate via stimulation of ß1-adrenoceptors on juxtaglomerular granular cells, increased renal tubular sodium reabsorption (decreased urinary sodium excretion) via stimulation of alpha1B- adrenoceptors on renal
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