Biochemical Mechanisms

Although the causes of DIT are not very clear, the mechanisms perhaps responsible for adaptive thermogenesis may be related to adenosine triphosphate (ATP) production and utilisation. In animal tissues, six different pathways for ATP production have been identified: two through anaerobic glycolysis of carbohydrates, one involving oxidative decarboxylation of carboxylic chetoacids, and three associated with electron transport to molecular oxygen. The energy required for ATP synthesis varies with the substrate considered, according to their different caloric value per 100 g, and to the yield in ATP per 100 g. The energy needed to produce 1 mol of ATP is therefore less for carbohydrates than for fats and proteins (Table 1).

Energy expenditure can be increased by increasing utilisation of ATP or by 'uncoupling' the tight relationship between fuel oxidation and biological work, allowing fuels to be oxidised in the absence of ATP consumption. ATP utilisation can be increased by physical activity and growth, or by processes referred to as 'futile cycles', in which ATP is consumed but net work is not per-

Table 1. Factors related to the energy available from ingested fats, carbohydrates and proteins. (Adapted from [4])

Fats

Carbohydrates

Protein

Mixed diet

Digestibility (%)

95

97

91

95

Conversion to

50.4

21.1

22.6

34.4

mol/100 g

nutrient

Costs

18.6

17.6

22.7

19

(Kcal/mol ATP)

Maximum

40

40

32-34

40

percent Kcal converted

to ATP

Diet-induced

3-4

10-15

15-30

10

thermogenesis (% of ingested Kcal)

ATP, adenosine triphosphate

ATP, adenosine triphosphate formed. Examples of futile cycles include the synthesis and degradation of proteins, the pumping and leakage of ions across membranes, and esteri-fication and lipolysis of fatty acids/triglycerides. Since the activity of these futile cycles is difficult to assess in intact organisms, it has been difficult to determinate their importance in adaptive ther-mogenesis. A clear example of uncoupling as a means of increasing energy expenditure is that brought about by uncoupling protein-1 (UCP1), a mitochondrial inner-membrane protein that leaks protons across the mitochondrial inner membrane. The energy that is stored in the mitochon-drial proton electrochemical gradient is released [8] in form of heat and is not used to synthesise ATP. UCP-1 is expressed at very high levels in BAT, the primary function of which is to produce heat in response to cold exposure. Other homologues of UCP-1 (UCP-2, UCP-3, UCP-4, and UCP-5) have been found in other tissues, but they do not appear to play an important role in regulating whole-body energy expenditure. The reason for the lack of effect of UCP homologues is presently unclear [9]. UCP-2 is distributed in skeletal muscle, white and brown adipose tissue, the gastrointestinal tract, lung, and the spleen; and UCP-3 in skeletal muscle. Other actions of uncoupling proteins seem to be the regulation of insulin secretion and the protection of free-radical oxygen species [10]. Insulin plays a role in mediating DIT and insulin resistance, and may therefore be implicated in the defective thermogenesis observed in diabetes.

Delicious Diabetic Recipes

Delicious Diabetic Recipes

This brilliant guide will teach you how to cook all those delicious recipes for people who have diabetes.

Get My Free Ebook


Post a comment