Blood fasting state

The normal values for thiamine in human blood vary from 25-80 mpg/ml (average of 27 cases), from 110-370 mfig/ml in urine (27 cases), and from 13-17 mpg/ml in cerebrospinal fluid (45 cases). These specimens were obtained from normal subjects, receiving no vitamin therapy and in the fasting state, to eliminate dietary influences. The... 

Since part of the inositol occurs in blood plasma in conjugated form, the sample must be hydrolyzed. This serves at the same time for depro-teinization. Ten milliliters of oxalated plasma obtained in the fasting state are hydrolyzed with 100 ml of 18% HC1 for 6 hours and the hydro-... 

Details of plasma lipoproteins and their metabolism are given in Section 5.5. Most of the cholesterol in the blood is carried as part of low density lipoprotein (LDL) or high density lipoprotein (HDL), whereas most triglyceride, in the fasting state, is carried by very low density lipoprotein (VLDL). The relative concentrations of these lipoproteins constitute the lipid profile and determine CVD risk. Diabetics are more likely to show an unhealthy profile with elevated concentrations of LDL and triglyceride but reduced HDL concentration. This pattern can be partly explained by enhanced fatty acid liberation from adipocytes as a consequence of insulin resistance in that tissue and due to reduced removal from the circulation of triglycerides, which is also insulin dependent. 

In the fasting state, resting muscle uses fatty acids derived from free fatty acids in the blood. Ketones maybe used if the fasting state is prolonged. 

Fig. 2 shows the serum verapamil levels of each volunteer in both the fasted and the fed states, and the position of the majority of pellets at each blood sampling. Especially large differences in time-concentration curves were noted if in the fasted state the majority of pellets had already entered the intestine at 2 h but in the fed state remained in the stomach for more than 4 h... 

In the fed state, the KB concentrations do not usually exceed 0.2 mmol/1, except during the neonatal period, where higher concentrations are observed. The level of ACAC increases more quickly than that of . The blood concentration of KBs increases during the fasted state, with an associated increase in the 30HB ACAC ratio, the result of PDH inhibition by mitochondrial acetyl CoA and NADH. KBs are primarily synthesised in the liver from acetyl CoA, the product of fatty acid oxidation. 

Patient preparation includes evaluation of clinical indications, and nutritional conditions (i.e. fed state, fast state, fasting duration) must be precisely defined. The patient must be fully informed of all procedures and at rest prior to blood sampling or invasive procedure. If fasting is required, the fast is scheduled for 24 h, but can be interrupted. Beginning at night, sampling is performed at 2,15, 20 and 24 h of the fast. 

Table 1.4.6 Reference values for blood lactate, pyruvate, ACAC and according to age, fed state and fasting state. L P lactate-.pyruvate ratio...

CM and VLDL secreted by intestinal cells and VLDL synthesized and secreted in the liver have similar metabolic fates. After secretion into the blood, newly formed CM and VLDL take up apoprotein (apo-C) from HDL and are subsequently removed from the blood (plasma half-life of less than 1 h in humans [137]) primarily by the action of lipoprotein lipase (LPL). Lipoprotein lipase is situated mainly in the vascular bed of the heart, skeletal muscle, and adipose tissue and catalyzes the breakdown of core TG to monoglycerides and free fatty acids, which are taken up into adjacent cells or recirculated in blood bound to albumin. The activity of LPL in the heart and skeletal muscle is inversely correlated with its activity in adipose tissue and is regulated by various hormones. Thus, in the fasted state, TG in CM and VLDL is preferentially delivered to the heart and skeletal muscle under the influence of adrenaline and glucagon, whereas in the fed state, insulin enhances LPL activity in adipose tissue, resulting in preferential uptake of TG into adipose tissue for storage as fat. 

Because insulin normally inhibits lipolysis, a diabetic has an extensive lipolytic activity in the adipose tissue. As is seen in Table 21.4, plasma fatty acid concentrations become remarkably high. /3-Oxidation activity in the liver increases because of a low insulin/glucagon ratio, acetyl-CoA carboxylase is relatively inactive and acyl-CoA-camitine acyltransferase is derepressed. /3-Oxidation produces acetyl-CoA which in turn generates ketone bodies. Ketosis is perhaps the most prominent feature of diabetes mellitus. Table 21.5 compares ketone body production and utilization in fasting and in diabetic individuals. It may be seen that, whereas in the fasting state ketone body production is roughly equal to excretion plus utilization, in diabetes this is not so. Ketone bodies therefore accumulate in diabetic blood. 

The liver also plays a central role in the regulation of lipid metabolism. When fuels are abundant, fatty acids derived from the diet or synthesized by the liver are esterified and secreted into the blood in the form of very low density lipoprotein (see Figure 30.15). However, in the fasting state, the liver converts fatty acids into ketone bodies. How is the fate of liver fatty acids determined The selection is made according to whether the fatty acids enter the mitochondrial... 

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