Fat oxidation

Another possible mechanism to explain the potential effect of dairy products on weight loss derives from the observation that intakes of dietary calcium and dairy products have been associated with increases in energy expenditure and a lowered respiratory quotient. A lower respiratory 

---

J (1999) Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in hiunans , AmJ Clin Nutr, 70, 1040-45. 

In addition to these interconversions, the metabolism of fat and the metabolism of carbohydrate are inseparably related. This fact is most clearly demonstrated by the appearance of such abnormal products of fat oxidation as the so-called ketone bodies in the blood and urine whenever the supply of carbohydrate is deficient or in cases where the organism is unable to metabolize this foodstuff. Whether ketonuria results because the metabolism of fat must occur concomitantly with that of D-glucose (ketolysis), or whether the presence of D-glucose prevents any fat breakdown because it is preferentially oxidized (antiketogenesis) is still a moot question. 

It is evident that even if acetic acid could be demonstrated as an intermediate in fat oxidation, the experimental data are quite preponderant in indicating that it would not be a D-glucose-former. 

Venables MC, Hulston CJ, Cox HR and Jeukendrup AE. 2008. Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. Am J Clin Nutr 87(3) 778-784. 

NM Emanuel, YN Lj askovskaja. Inhibition of Fat Oxidation. Moscow Pistsheprom-isdat, 1961 (in Russian). 

However, it should be noted that although fat oxidation provides quantitatively more ATP than does the oxidation of glucose, the rate at which ATP is generated via 13-oxidation is slower than the rate of generation by glycolysis a fact which explains why glucose is the preferred fuel during sudden bursts of muscular activity when ATP concentration need to be topped-up rapidly. 

During low-intensity exercise, fat oxidation predominates as the energy source with some contribution by glucose. 

During sustained exercise, fat oxidation alone cannot provide sufficient ATP to maintain a high power output (see Chapter 13). 

In an adult, it is only after about 24 hours of fasting or during prolonged physical activity that fatty acid oxidation plays a major role in energy provision. Neither condition is common in developed countries, so that an inability to generate ATP from fat oxidation is not normally apparent. 

Figure 8.9 The ATP produced from oxidation of half of the amino acids is used to synthesise glucose from the other half of the amino acids. This is a general metaboiic point, it does not appiy in aii conditions the ATP can be used in other processes (e.g. urea cycie). In starvation, ATP is generated from fat oxidation, since oxoacids are not oxidised but are converted to giucose.

As the duration of low-intensity exercise increases, the contribution of fat oxidation to ATP generation rises and parallels the reduced contribution of glycogen (Table 13.7). For very prolonged activities, when aU the muscle and fiver glycogen has been used, fatty acids become the only fuel available. However, fatty acid oxidation can generate ATP that no more than the rate provides about 60% of which... 

The increased mobilisation of fatty acids from adipose tissue raises the plasma concentration, which increases the rate of fat oxidation by muscle. It also releases some essential fatty acids from the store in the triacylglycerol in adipose tissue. These are required for formation of new membranes in proliferating cells and those involved in repairing the wound (e.g. fibroblasts) (Chapters 11 and 21 Figure 21.22). 

Wolfe has presented an excellent description of the systematic application of stable and radioactive isotope tracers in determining the kinetics of substrate oxidation, carbon dioxide formation (including C02 breath tests), glucose oxidation, and fat oxidation in normal and diseased states. Quantification of the rate and extent of substrate oxidation can be achieved by using a specific or C-substrate which upon oxidation releases radioactive carbon dioxide. 

Possibly a signaling molecule which can help fight weight gain utilized by the key enzymes that control fat oxidation, at extraordinarily high rates... 

Besides the well-known Maillard reaction, additional reactions like sugar degradation, fat oxidation and interaction of Maillard intermediates are major sources for powerful flavour materials. 

Roe CR, Sweetman L, Roe DS, David F, Brunengraber H (2002) Treatment of cardiomyopathy and rhabdomyolysis in long-chain fat oxidation disorders using an anaplerotic odd-chain triglyceride. J Clin Invest 110 259-269... 

Therefore, the metabolite interferes with mitochondrial function and decreases the production of ATP and other important cofactors such as NADH and FADH. Therefore, after repeated use of the drug, mitochondrial integrity is reduced and cellular and overall liver fat oxidation is inhibited. Consequently, fat accumulates, seen as microvesicular steatosis. Electron microscopy shows swollen mitochondria and damaged mitochondrial structures. The accumulated lipid may encourage lipid peroxidation and oxidative stress to occur, causing further damage. 

Advanced review of metabolic defects in fat oxidation, including MCAD mutations. 

---