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In this regard, we have previously suggested that uric acid may have had a significant role in mediating the marked rise in hypertension prevalence that has occurred worldwide [ 42 ]. Over the last century, there has been a dramatic increase in the ingestion of added sugars which contain fructose, and the increased consumption of added sugars correlates both with higher serum uric acid levels and with elevated blood pressure [ 43,44 ]. Administering high doses of fructose to humans raises uric acid levels and blood pressure, and preventing the rise in uric acid with allopurinol prevents the increase in blood pressure [ 45 ]. Diets restricting fructose also lower uric acid levels and blood pressure (M. Madero, submitted). Mean serum uric acid levels are also increasing in our population in association with the rise in fructose ingestion and increasing prevalence of hypertension, and numerous studies have found that elevated uric acid could predict the development of hypertension [ 46,47 ]. Additionally, several small clinical trials have reported that lowering uric acid could reduce blood pressure in humans, including a recent prospective double-blind trial in obese adolescents [ 48–50 ]. Clearly, additional studies are required to confirm these findings.

As mentioned, a number of epidemiologic and experimental studies have shown that increased dietary fructose intake, particularly in the form of high-fructose corn syrup, (HFCS) is associated with development of hyperuricaemia. The precise mechanism by which fructose causes an increase in uric acid relates to its unique metabolism. The initial phosphorylation of fructose to fructose-1-phosphate by fructokinase results in adenosine triphosphate (ATP) consumption. Unlike glucokinase, which has a negative feedback to prevent excessive phosphorylation and ATP depletion, the phosphorylation of fructose will proceed until all fructose is phosphorylated. During this process, intracellular phosphate falls, and adenosine monophosphate (AMP) deaminase is stimulated, which results in the production of inosine monophosphate (IMP) and eventually uric acid. Intracellular uric acid rises followed by a rise in serum uric acid that peaks at ~ 30min [ 51,52 ]. With high levels of fructose ingestion, even fasting levels of uric acid will rise, consistent with epidemiological studies linking fructose intake with hyperuricaemia [ 53 ].

The arterioles have a major role in protecting distal organs from the elevated pressure present in the central circulation. In the kidney, this autoregulatory vasoconstrictive response is critical in preventing transmission of pressure to the glomeruli and peritubular capillary bed. Bidani and Griffin have provided convincing evidence that an altered renal autoregulatory response is commonly present in chronic kidney disease, and that this leads to increased transmission of systemic pressure to the glomeruli [ 54 ]. An insight into the mechanism was provided by the laboratory of the late Jaime Herrera-Acosta, who showed that the development of afferent arteriolar disease resulted in impaired autoregulation and glomerular hypertension [ 14 ]. Importantly, this group showed that if the arteriolosclerosis could be prevented and renal autoregulation remained intact, the progression of renal disease could be halted [ 14 ]. The mechanism is relatively logical, for the diseased arterioles have been shown to have an increase in collagen content [ 10 ] and hence are not expected to vasoconstrict or vasodilate as quickly or as efficiently as normal arterioles. We have suggested that the consequences of altering the autoregulatory mechanisms of the arteriocapillary bed may be critical as a risk factor for end-organ damage, particularly by increasing the risk for progression of renal disease [ 14 ]. This concept has also been proposed for the impairment of brain function by Thompson and Hakim in a recent publication [ 55 ].

We have examined the possible roles of adipokines versus FFAs in the insulin resistance of the fat-fed canine model ( 33 ). To our surprise, we did not see increases in the enzyme expressions of several potential adipokines in visceral fat, despite the onset of insulin resistance in the fat-fed model. In contrast, we measured changes in expression of enzymes related to the visceral turnover of FFAs consistent with the release of FFAs into the portal vein in the insulin-resistant state ( Figure 2 ). Also, we observed significant deposition of triacylglycerols in the liver, which suggests the transport of FFAs from the visceral depot to the liver. These data show that FFAs could be responsible for the hepatic insulin resistance observed with elevated fat intake in the dog model. However, data that fasting FFA concentrations change little during fat feeding (which were confirmed in our experiments) appear to discount the importance of FFAs. However, further studies have supported the role of FFAs in the development of insulin resistance.

Figure 2
FIGURE 2.
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Changes in gene expression with the development of visceral adiposity in the fat-fed dog model. CPT-1, carnitine palmitoyltransferase-1; FABP, fatty acid binding protein; FFA, free fatty acids; G6Pase, glucose-6-phosphatase; HSL, hormone sensitive lipase; IL-6, interleukin-6; LPL, lipoprotein lipase; PEPCK, phosphoenolpyruvate carboxykinase; PPARγ, peroxisome proliferator-activated receptor-γ; SREBP-1, sterol regulatory element-binding transcription factor-1; TNF-α, tumor necrosis factor-α.

FIGURE 2.
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Changes in gene expression with the development of visceral adiposity in the fat-fed dog model. CPT-1, carnitine palmitoyltransferase-1; FABP, fatty acid binding protein; FFA, free fatty acids; G6Pase, glucose-6-phosphatase; HSL, hormone sensitive lipase; IL-6, interleukin-6; LPL, lipoprotein lipase; PEPCK, phosphoenolpyruvate carboxykinase; PPARγ, peroxisome proliferator-activated receptor-γ; SREBP-1, sterol regulatory element-binding transcription factor-1; TNF-α, tumor necrosis factor-α.

The relation between obesity and hypertension led Landsberg et al ( 34 ) to propose that obesity activates the sympathetic nervous system. Experiments done in our laboratory, in which we measured directly the rate of release of FFAs from the omental adipose depot (by using arteriovenous differences), showed the pulsatile nature of such release ( 35 ). In fact, we observed a burst of lipolysis (coordinated net portal appearance of FFAs and glycerol) every 10–11 min in the fasting state. These pulses were almost totally suppressed by the high-affinity β-3 blocking agent bupranolol ( 36 ). Thus, it is apparent that the sympathetic nervous system is responsible for at least part of the visceral lipolysis in the fasting state. In recent studies, we observed that pulsatile octanoate is more potent than constant FFA administration in stimulating endogenous (hepatic) glucose production ( 37 ). Therefore, it is reasonable to suppose that the sympathetic nervous system plays a role in the pathogenesis of temporal increases in FFAs in blood, which in turn may render the liver resistant to insulin.

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