The regulated uncoupling of oxidative phosphorylation is a biologically useful means of generating heat. The uncoupling of oxidative phosphorylation is a means of generating heat to maintain body temperature in hibernating animals, in some newborn animals (including human beings), and in mammals adapted to cold. Brown adipose tissue, which is very rich in mitochondria (often referred to as brown fat mitochondria), is specialized for this process of non shivering thermogenesis. The inner mitochondrial membrane of these mitochondria contains a large amount of uncoupling protein (UCP), here UCP-1, or Thermogenin, a dimer of 33-kd subunits that resembles ATP-ADP translocase. UCP-1 forms a pathway for the flow of protons from the cytosol to the matrix. In essence, UCP-1 generates heat by short-circuiting the mitochondrial proton battery. This UCP-1 channel is activated by fatty acids (as in the given case) – Figure-2.
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Because of the adverse side effects associated with high doses of niacin (see Safety ), it has most often been used in combination with other lipid-lowering medications in slightly lower doses (54) . In particular, LDL cholesterol-lowering statins like simvastatin form the cornerstone of treatment of hyperlipidemia , a major risk factor for CHD. The HDL- Atherosclerosis Treatment Study (HATS), a three-year randomized controlled trial in 160 patients with documented CHD and low HDL levels found that a combination of simvastatin and niacin (2 to 3 grams/day) increased HDL levels, inhibited the progression of coronary artery stenosis (narrowing), and decreased the frequency of cardiovascular events, including myocardial infarction and stroke (58) . Patients with metabolic syndrome display a number of metabolic disorders, including dyslipidemia and insulin resistance , that put them at increased risk for type 2 diabetes mellitus , cardiovascular disease, and mortality. A subgroup analysis of the HATS patients with metabolic syndrome showed a reduction in rate of primary clinical events even though glucose and insulin metabolism were moderately impaired by niacin (59) . Moreover, a review of niacin safety and tolerability among the HATS subjects showed glycemic control in diabetic patients returned to pretreatment values following eight months of disease management with medication and diet (60) . Similarly, the cardiovascular benefit of long-term niacin therapy outweighed the modest increase in risk of newly onset type 2 diabetes in patients from the CDP study (61) .