Glucose causes

Shiau et al. [73] directly measured the microclimate pH, pHm, to be 5.2-6.7 in different sections of the intestine (very reproducible values in a given segment) covered with the normal mucus layer, as the luminal (bulk) pH, pH/, was maintained at 7.2. Good controls ruled out pH electrode artifacts. With the mucus layer washed off, pHm rose from 5.4 to 7.2. Values of pHfo as low as 3 and as high as 10 remarkably did not affect values of pHm. Glucose did not affect pHm when the microclimate was established. However, when the mucus layer had been washed off and pHm was allowed to rise to pHfo, the addition of 28 mM glucose caused the original low pHm to be reestablished after 5 min. Shiau et al. [73] hypothesized that the mucus layer was an ampholyte (of considerable pH buffer capacity) that created the pH acid microclimate. 

As noted previously, available therapies moderate the hyperglycemia of diabetes, but fail to completely normalize metabolism. The long-stand-hg elevation of blood glucose causes the chronic complications of diabetes—premature atherosclerosis, retinopathy, nephropathy, and neuropathy. Intensive treatment with insulin (see p. 339) delays the onset and slows the progression of these long-term complications. For example, the incidence of retinopathy decreases as control of blood glu-... 

Correct answer = A. The addition of glucose causes cyclic AMP production to decrease. In the absence of cyclic AMP, the CAP protein cannot remain bound to its DNA binding site. An empty CAP binding site is not able to help RNA polymerase initiate transcription, so the rate of transcription decreases. Lower mRNA produc tion results in decreased P-galactosidase syn thesis. Because lactose is still present, the inducer (allolactose) remains bound to the repressor, which continues to be unable to bind to the operator. 

Available treatments for diabetes moderate the hyperglycemia, but fail to completely nor malize metabolism. The long-standing elevation of blood glucose causes the chronic com plications of diabetes—premature atherosclerosis, retinopathy, nephropathy, and neuropathy. 

T. reesei, a saprophytic fungus, is capable of utilizing a variety of carbohydrates. Yet, only a few carbohydrates induce cellulase production. Inducers include cellulose, cellulose derivatives, lactose, and sophorose (31,32). Mandels and Reese (31,32) studied the inducibility of various sugars and found that sophorose is an excellent cellulase inducer in T. reesei while having little effect in other fungi or bacteria. On further examination they found that trace amounts of sophorose present in glucose caused the apparent ability of glucose to be a cellulase inducer in T. reesei. 

In eight patients with type 2 diabetes and seven matched non-diabetics, subcutaneous glucagon-like pep-tide-1 and intravenous glucose caused reactive hypoglycemia in five controls but not in the patients (10). Glucagon was suppressed. 

When complex I is defective, there is an excess of cellular NADH, which pushes the lactate dehydrogenase to form lactate from pyruvate (anaerobic glycolysis). This results in higher than normal utilization of glucose, causing hypoglycemia. Because succinate is oxidized at the complex II level, its oxidation is not affected. 

MK-912 (L-657,743) (14), an analogue of yohimbine with high in vitro potency and high a,2/ai selectivity [89, 90], lowers FPG and improves glucose tolerance in ob/ob mice and reversed the inhibition of GIR by clonidine [91]. In man, MK-912 attenuated the small elevation in blood glucose caused by clonidine, but had no significant effect on insulin concentration [92]. Healthy volunteers [93] and NIDDM patients [94] treated with MK-912 exhibited a small increase in basal insulin level and a modest decrease in FPG while substantial increases in catecholamines and... 

It is usually easier to differentiate hypoglycaemia from severe diabetic ketosis than from other causes of coma, which are as likely in a diabetic as in anyone else. It is unsound to advocate blind administration of i.v. glucose to comatose diabetics on the basis that it will revive them if they are hypoglycaemic and do no harm if they are hyper-glycaemic. A minority of comatose insulin-dependent diabetics have hyperkalaemia and added glucose can cause a brisk and potentially hazardous rise in serum potassium (mechanism uncertain), in contrast to nondiabetics in whom glucose causes a fall in serum potassium. 

FIGURE 16.4 Schematic diagram showing the effect of competing glucose causing a gel to sol transition and increasing solute diffusion. 

For glucose solutions, typically, the ratios of forms are 36% a, 63% p, <1% open chain. When you dissolve glucose in water, the slow cdnversion of the solid equilibrium mixture to the aqueous equilibrium mixture means that the rotation glucose causes to polarised light decreases (becomes less positive) over time. This is called mutarotation. 

Glucose causes cAMP levels in the cells to decrease. 

In continuous ambulatory peritoneal dialysis, the use of a peritoneal solution with 4.25% glucose caused plasma glucose levels to reach above 5.5 mmol/liter for 4 hours during the dialysis session and produced a marked insulin response (A12). It is probable that Hb Aj. values would be somewhat elevated in such subjects, but this would not occur with the use of 1.5% glucose solutions. 

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