8.3.0.0 Maturity-‍Onset Di­a­betes of the Young

MODY is fre­quent­ly char­ac­ter­ized by onset of hy­per­glycemia at an early age (clas­sically be­fore age 25 years, al­though di­ag­no­sis may occur at older ages). MODY is char­ac­ter­ized by im­paired in­sulin se­cre­tion with min­i­mal or no de­fects in in­sulin ac­tion (in the ab­sence of co­ex­is­tent obe­si­ty). It is in­her­it­ed in an au­to­so­mal dom­i­nant pat­tern with abnor­malities in at least 13 genes on dif­ferent chro­mo­somes iden­tified to date. The most com­monly re­port­ed forms are GCK-‍MODY (MODY2), HNF1A-‍MODY (MODY3), and HNF4A-‍MODY (MODY1).

Clin­i­cally, pa­tients with GCK-‍MODY ex­hib­it mild, sta­ble, fast­ing hy­per­glycemia and do not re­quire antihy­per­glycemic ther­a­py ex­cept some­times dur­ing preg­nan­cy. Pa­tients with HNF1A- or HNF4A-‍MODY usu­al­ly re­spond well to low doses of sul­fony­lureas, which are con­sid­ered first-‍line ther­a­py. Mu­ta­tions or dele­tions in HNF1B are as­so­ci­at­ed with renal cysts and uter­ine mal­for­ma­tions (renal cysts and di­a­betes [RCAD] syn­drome). Other ex­treme­ly rare forms of MODY have been re­port­ed to in­volve other tran­scrip­tion fac­tor genes in­clud­ing PDX1 (IPF1) and NEU­ROD1.