Uncoupled heating: Warthogs lack brown fat & live in burrows.

One obvious reason why warthogs live in burrows is to escape from their predators. But another important reason is for temperature control and in particular to keep warm in the cold months (1).

Temperature in animals is regulated by changes in heat input & or output (see earlier blog on temperature regulation). The input can be from exogenous sources e.g. radiation from the sun or endogenous sources e.g. basal body metabolism, shivering. The output can also be altered by decreasing exogenous loss e.g. cutting down conduction, convection, evaporative, or radiant losses by behavioral (e.g. sheltering in nests) or physiological (e.g. vasoconstriction, piloerection) means.

A previously discussed in the blogs on temperature regulation endothermic animals e.g. mammals regulate their temperature varying the heat input by altering the rate of cell metabolism. Most of the energy production in cells occurs when glucose & fats are oxidized in the mitochondria. The mitochondria are the cells “powerhouses” burning food to release energy (Figure 1).

This is the powerhouse of the cells

This is the powerhouse of the cells (click to enlarge)

The energy is stored as ATP to be used later to power cell functions e.g. muscle contractions or released as heat. Basal energy metabolism always produces heat as the production of energy by oxidation of glucose & fat is only 60% efficient and the heat produced (i.e. from 40% of energy produced) is an essential mechanism for maintaining body temperature at 37oC. In cold conditions this basal heat production may be insufficient to maintain the temperature at 37oC & endothermic animals can compensate by increasing cell metabolism. In adults this is done mainly by shivering (non-coordinated contractions of muscle fibers) and in most newborn & young animals by mainly thermogenesis in brown fat.  The human baby is unable to shiver & depends entirely on the “brown fat” running down the spinal area. These brown fat cells, unlike white fat cells, are densely filled with mitochondria which when stimulated by adrenalin metabolize glucose & fats to produce heat. Brown fat has that color because of its rich blood supply and the iron containing cytochrome compounds in its many mitochondria.

A useful analogy is that white fat acts as a woolen blanket i.e. reduces heat output by insulation & brown fat increases heat production (input) acting as an “electric” blanket i.e. non-shivering thermogenesis.

Heat production in Brown fat: Energy in all cells is derived from the break down (catabolism) of mainly glucose and fatty acids by oxidation. The atoms i.e. hydrogen, carbon, oxygen in these molecules are linked together by high energy bonds. When the molecule is catabolized by oxidation up this energy is released and captured as phosphate containing molecules (ATP i.e. adenosine triphosphate) for use by all cell processes.

Glucose + oxygen→ carbon dioxide + water + energy (ATP & heat)

When glucose is burnt in air its energy is rapidly released as heat as the glucose is oxidized by oxygen. In the cells the glucose is also oxidized but the energy released in a chain of small steps allowing a large percentage of the energy to be captured & stored as ATP (adenosine molecule linked to three (“tri”) phosphates). ATP can be seen as the battery that powers all cell processes & must continuously be replenished. This recharging is “oxidative phosphorylation”: glucose & lipids are oxidized & the adenosine is phosphorylated with most of the energy being stored in the last of its 3 phosphate bonds

After initial break down in the cell cytoplasm downstream products pass into the mitochondria, with its double lipid membrane wall. In this organelle most of the ATP is produced via the Kreb’s (citric) cycle (Figure 2).

Production of ATP by oxidative phosphorylation (click to enlarge)

Production of ATP by oxidative phosphorylation (click to enlarge)

The products pass around the cycle passing from one enzyme & coenzyme (derived from vitamins) to another. At some steps carbon dioxide is removed and this must be excreted via the lungs. At others they are oxidized by removal of a hydrogen atom (proton plus its electron) which passes to carrier molecules the coenzymes FAD & NAD (synthesized from vitamins). These transport molecules pass on the hydrogen atoms to the enzymes of the electron ladder present in the inner membrane of the mitochondria (Figure 2). Here the pass along a complex chain of enzymes called the electron ladder. The electron is split off from the hydrogen atom & the resulting hydrogen proton is pumped into the space between the inner & outer membranes from the hydrogen proton. The electron passes along various enzymes of the electron ladder e.g. cytochromes embedded in the inner membrane by sequential reduction oxidation reactions until it is finally passed onto oxygen & water is produced. Thus a concentration gradient of hydrogen protons is built up in the inter-membrane space. The electrons finally reduce oxygen to water & the large proton concentration that has built up pass back into the inner mitochondrial space via a protein ATP synthase. The latter phase produces the ATP & the analogy has been made of a dam where water now flows out via a turbine motor to produce energy (Figure 2). The hydrogen protons flow into the ATP synthase with its protein blades & the stream turns the protein on its axis, with the energy produced being used to synthesize ATP from ADP & phosphate. There are many video lessons of this process now available via “You Tube”.

In summary in normal cell metabolism the energy produced by electron ladder & proton pump is coupled with the production of ATP. However in brown fat there is a protein in the inner mitochondrial membrane that uncouples the energy released by electron release from the proton stream to produce ATP (Figure 3).

The uncoupling of oxidation from phosphorylation in mitochondria results in more heat production. The role of the uncoupling protein. (click to enlarge)

The uncoupling of oxidation from phosphorylation in mitochondria results in more heat production. The role of the uncoupling protein. (click to enlarge)

This results in all the energy being release by turned to heat. This uncoupling protein UCP1 Is only found in brown fat, and the hydrogen ions in the inter-membrane space flow back into the matrix of the mitochondrion via this protein thus by passing the ATP synthase turbine. The energy released by the flow is not coupled to ATP production and released as heat i.e. brown fat is a heat producing organ (2).

It is well recognized that all piglets e.g. warthogs are prone to cold.  Recent research shows that warthogs do not have white fat (personal communication Hoffman L & Swanepoel M, University of Stellenbosch, South Africa); the opposite is stated on many websites. But it is true they have sparse hair over their bodies. In pig breeding artificial heating via radiant lamps is provided while warthogs build their best in empty aardvark & porcupine burrows to prevent heat loss. It is interesting to note that piglets can shiver; it would be of interesting to know if there is an inverse relationship between the two methods of heat production in other newborn mammals. In human babies the brown fat compensates for the lack of their ability to shiver. The warthogs are diurnal animals & at night sleep together in burrows to keep warm. The piglets only leave the burrows after 6 weeks.

In 2005 research into the pig genome revealed a fascinating  fact. Even though pigs do not have brown fat they still have the gene to produce the uncoupling protein. However the gene is nonfunctional because of various mutations & deletions. This confirmed earlier morphological studies showing that, unlike all other newborn mammals, that pigs do not have brown fat. The lack of this electric blanket (non shivering thermogenesis) is the reason for the susceptibility of piglets to cold. It helps explain why warthogs are the only hoofed animals that build nests in burrows. It is not known which came first, the mutations in the UCP1 gene or the loss of the brown fat. Phylogenetic studies show that the UCP1 gene was disrupted 20 million years ago!  Finally it is interesting to note that origin of brown fat appears to be more closely related to that of muscle cells than white fat cells (3).


1. Sowls LK & Phelps RJ. Body Temperatures of Juvenile Warthogs & Bushpigs. Journal Mammalogy. 1966;47:134-137

2. Berg F et al. The uncoupling protein 1 gene (UCP1) is disrupted in the pig lineage: A genetic explanation for poor thermoregulation in piglets. PLoS Genet 2006;2:1178-1181

3. Cannon B, Nedergaard J. Neither brown nor white. Nature 2012;488:286-287

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