Abstract

Iron constitutes an essential element that is implicated innumerous physiological functions. In the context of the pancreatic β cells, they act as components of the Fe –S cluster proteins, which are a must for the appropriate insulin generation and processing. As far as mitochondria are concerned , in the form of a constituent of the respiratory chain it aids in the generation of ATP along with Reactive oxygen species(ROS),that result in induction of β cells depolarization that causes potentiation of insulin liberation that is calcium based .It is of great importance that a marked fiine tuning gets established with regards to the iron cellular amounts to guarantee normal provision of Iron along with avoidance of iron overload. Actually, in view of the great reaction with oxygen in addition to the generation of free radicals , iron overload might result in Oxidative injury of cells that possess susceptibility to this situations in view of the normal escalation of ROS development besides lesser availability of antioxidant enzymes action .Thus here we conducted a systematic review utilizing usual search engine utilizing the MeSH; iron metabolism; DM; haemochromatosis; thallasemia; Alzheimer’s ;Parkinson’s disease ; Friedrich’s ataxia; Iron homeostasis; Iron binding protein; transferrin bound iron(TBI); non TBINTBI); Divalentmetal transporter I(DMT1); ferroportin; islet amyloid polypeptide; zinc transporter ZIP 14; Chaperone proteins- poly CR binding proteins(PCBPs); mitoferrin(Mfrn); Fe-S clusters - enzyme CDKAL1; hepcidin; hephaestin; frataxin ; labile iron pool (LIP); ABCT7; PDX1;MafA; PHD; MAMs; Miner 1;gestational DM; ferroptosis; ferroportin; iron overload &treatment ;toxicity in brain, GIT; from 1980 till 2022 till date. We found a total of 4500 articles out of which we selected 135 articles for this review. No meta-analysis was done. Main aim of this review was to get a better insight in mode of iron homeostasis in β cells, with mode of changed in this event in their damage. How abnormal iron storage/chaperon proteins might cause diabetes.

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