Use of the additional need to remove amino nitrogen. The elimination
Use of the additional need to remove amino nitrogen. The elimination of excess glucose also poses a few problems by itself. Glucose is the main inter-organ energy staple, and PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26552366 is released in large amounts by the intestine-portal vein-liver system because the main dietary component is supposed to be starch, which digestion yields glucose. The absence of dietary glucose is a physiological signal in itself, a correlate of starvation, and elicits the mobilization of lipid stores [16,17] to cover the body energy needs. Thus, high lipid availability is construed as a sham “starvation-like condition”, which prevents the massive oxidation of glucose [18]. Evidently, excess lipid availability because consumption of high-fat diets is not akin to real starvation or energy deficit, but the preservation of glucose stands; furthermore, high glucose and energy availability enhance the protection of dietary amino acids (paradoxically also in excess) from their utilization as energy substrates [19,20]. The combination of excess fatty acids and excess glucose poses a serious problem to the homoeostatic maintenance of energy balance, a condition unique to the metabolic syndrome (MS) [21,22]. The body has to find ways to circumvent the strict glucose preservation measures painstakingly developed and established through evolution for its own protection, such as insulin resistance [23,24]. In the present review, these processes and effects are shown as both homoeostatic control systems and pathogenic mechanisms in the development of the metabolic syndrome,Excess glucose and insulin resistanceAfter insulin resistance denies its entry to muscle, and decreased blood flow restricts adipose tissue uptake, most of the remaining glucose could only be used in significant amounts by BAT (to sustain thermogenesis and for lipid storage) [25], or by the liver, the intestine and -perhaps- by the microbiota. The liver capacity to eliminate excess glucose is limited because of space availability constrictions to glycogen and lipid storage [26]. However, lipogenesis has to be carried out, even countercurrent, because of an already large excess of dietary fatty acids and triacylglycerols, temporarily stored in the liver, waiting for their eventual release as VLDL. A large excess of non-exported energy (lipid, glucose) may help induce liver steatosis, damaging liver function [27]. High insulin helps drive excess glucose towards lipogenesis [28], but the process is also limited by the already excessive availability of acetyl-CoA, which cannot be converted into ketone bodies via 3-hydroxy-3-methyl-glutaryl-CoA because the high levels of glucose fully inhibit the ketone pathway [29]. As a consequence, glucose levels keep rising and/or are maintained high. Let’s look now where the unwanted glucose may go. BAT enhanced consumption of glucose may represent a quantitatively significant possibility for rodents, but it is BQ-123MedChemExpress BQ-123 doubtful that in humans, with a limited BAT presence [30,31], it may represent a significant dent in the pool of excess circulating glucose, especially when BAT preferred substrate is, again, lipid [32]. Excess glucose becomes a danger by itself: can affect water balance because of its osmotic properties [33], and increase the glycation (and consequent loss in function) of a number of proteins, especially those in contact with the bloodstream [34]. Thus, over a certain limit, excess glucose may be lost via urine. However, before these drastic measures are taken, the b.