Normally, when insulin binds to the extracellular alpha chain of the insulin-receptor, it originates a change within receptor’s structure, resulting in autophosphorylation of particular tyrosines in the cytoplasmic part of the beta chains. This change causes an initiation of a multifaceted cascade, which lastly results in secretion of the insulin.
It is a well-known fact that the determination of any function of a protein is dependent on the sequence of the amino acids. Obviously any changes in the sequence result in differed function. This change is called as mutation. It is an established fact that missense mutations in the tyrosine kinase portion of the insulin receptor gene are present in patients with NIDDM. This mutation in the insulin-receptor prevents the relay of the stimuli, resulting in inhibition of insulin secretion finally.
Here, we have demonstrated that the mutations in tyrosine kinase portion of insulin receptor gene found in the patients of NIDDM, are actually the derangement in the ruksa, laghu attributes, which are due to the combination of Vayu mahabhuta and Akash mahabhuta. We have also concluded that the replacement of Vayu mahabhuta and Akash mahabhuta by Prithvi mahabhuta and Jala mahabhuta, is the backbone of the pathology in NIDDM.