Metabolism is the set of chemical reactions that happen in the day to day lives of living organisms in order to maintain their lives. The processes allow the organisms to respond to their environment by growing and reproducing and finally maintaining their structure. Catabolism which breaks down organic matter to harvest energy and anabolism which uses the energy to construct cell components both constitute metabolism. Metabolism is the intracellular process that consumes substrates and produces by-products in the course of generating chemically stored energy for anabolism (Prosser & Brown, 1961).
Intracellular calcium has a vital role in the metabolic derangements mainly associated with obesity. The increase of intracellular calcium through stimulating the receptor mediated calcium channels also has clearly shown to stimulate the functioning and activity of fatty acid synthase (FAS). Fatty acid synthase is a major enzyme de novo lipogenesis that inhibits both basal and agonist-stimulated lipolysis in human and murine adipocytes. Leptin increases basal and insulin-stimulated glucose uptake into human subcutaneous adipocytes (Bray & Bouchard, 2004). Calcium channel antagonism can reverse these effects. It therefore means that increasing the level of [Ca2+]i promotes the accumulation of triglyceride in adipocytes. It exerts a coordinated control over both lipogenesis and lipolysis, and serves to simultaneously stimulate the former and suppress the later so as to give lipid fillings and adipocyte hypertrophy.
Intracellular calcium has also to a greater extent been implicated to regulate adipogenesis which is thought to contribute to human and murine obesity. Increasing intracellular calcium by either reducing Ca2+-ATPase or increasing Ca2+ influx, inhibits the early stages of murine adipocyte differentiation. Further, it comes with an inhibitory effect in murine adipocyte differentiation to mature adipocytes and also acts as a signaling factor in regulating adipocyte metabolism.
In the early stages of heart failure disease, action potential prolongation may at times increase the aptitude of intracellular calcium transient which causes positive inotropy. In the severe hypertrophy and the end-stage heart failure, despite the continued action potential prolongation, the calcium transient aptitude is severely reduced. This mechanism involves the reduced expression of calcium handling proteins and the late events may at times herald the onset of failure. Altered calcium handling is a finding of human and animal heart failure.
Intracellular calcium is known to increase outward current in cardiac muscle. It is interesting to know the possibility of calcium activated currents in the heart and other muscles; this is because the cells have intracellular stores that function to release calcium. The apparent complexity of membrane currents in the muscle may be explained as a manifestation of excitation contraction coupling. Intracellular calcium has a vital role in controlling the transient outward current which underlines the early repolarisation in the cardiac Purkinje fibers. Therefore, blockers of calcium current inhibit the transient outward current that varies directly with the external calcium concentration.
Intracellular transport- Calcium is responsible in the migration and movement of intracellular organelles which include receptors and vesicles. It also determines and important part in secretions and exocytosis. In cytoplasmic enzymes, calcium acts by first activating the various protein kinases like the protein kinase C, A2 phospholipase, calmodulin and calpain that hydrolyzes many proteins. In the mitochondrial enzymes, increasing the intramitochondrial calcium will activate deshydrogenases that is responsible for transforming acetate to pyruvate. In summary, an increase in intramitochondrial calcium will activate the Krebs cycle which finally increases the synthesis of ATP.
In conclusion, the presence of calcium is of great importance in the functioning of the cell but if in excess quantities it has some destructive effects. In the case where the glutamate receptors are over stimulated, the increase in the intracellular calcium brings about hyper contracture of the smooth muscle and hyper-activation of the enzymes like the phospholipases. At neurons level, the T and N type channels by which calcium goes to the neurons take part in their polarization.