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In this review we summarise the current understanding of the relationship between iron homoeostasis and metabolic disease.

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Functional analyses demonstrated that i ) DIV-1 is required for the robust proliferation typical of the germline, ii ) loss of DIV-1 enhances and suppresses specific phenotypes that are associated with reduced and elevated GLP-1/Notch activity in germline and somatic tissues, and iii ) DIV-1 works together with FBF/PUF proteins, downstream regulators of GLP-1/Notch signaling, to promote germline stem cell (GSC) maintenance and germline proliferation

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