4.3.0.0 Type 2 Di­a­betes

Type 2 di­a­betes, pre­vi­ous­ly re­ferred to as “nonin­sulin-‍de­pen­dent di­a­betes” or “adult-‍onset di­a­betes,” ac­counts for 90– 95% of all di­a­betes. This form en­com­pass­es in­di­vid­u­als who have rel­a­tive (rather than ab­so­lute) in­sulin deficien­cy and have pe­riph­er­al in­sulin re­sis­tance. At least ini­tially, and often through­out their life­time, these in­di­vid­u­als may not need in­sulin treat­ment to sur­vive.

There are var­i­ous caus­es of type 2 di­a­betes. Al­though the specific eti­olo­gies are not known, au­toim­mune de­struc­tion of β-‍cells does not occur and pa­tients do not have any of the other known caus­es of di­a­betes. Most but not all pa­tients with type 2 di­a­betes are over­weight or obese. Ex­cess weight it­self caus­es some de­gree of in­sulin re­sis­tance. Pa­tients who are not obese or over­weight by tra­di­tion­al weight cri­te­ria may have an in­creased per­cent­age of body fat dis­tribut­ed pre­dom­i­nant­ly in the ab­dom­i­nal region.

DKA sel­dom oc­curs spon­ta­neous­ly in type 2 di­a­betes; when seen, it usu­al­ly aris­es in as­so­ci­a­tion with the stress of an­oth­er ill­ness such as in­fec­tion or with the use of cer­tain drugs (e.g., cor­ti­cos­teroids, atyp­i­cal an­tipsy­chotics, and sodi­um–glu­cose co­trans­porter 2 in­hibitors) (45,46). Type 2 di­a­betes fre­quent­ly goes undi­ag­nosed for many years be­cause hy­per­glycemia de­vel­ops grad­u­al­ly and, at ear­li­er stages, is often not se­vere enough for the pa­tient to no­tice the clas­sic di­a­betes symp­toms. Nev­er­the­less, even undi­ag­nosed pa­tients are at in­creased risk of de­vel­op­ing macrovas­cu­lar and mi­crovas­cu­lar com­pli­ca­tions.

Whe­re­as pa­tients with type 2 di­a­betes may have in­sulin lev­els that ap­pear nor­mal or el­e­vat­ed, the high­er blood glu­cose lev­els in these pa­tients would be ex­pect­ed to re­sult in even high­er in­sulin val­ues had their β-cell func­tion been nor­mal. Thus, in­sulin se­cre­tion is de­fec­tive in these pa­tients and insufficient to com­pen­sate for in­sulin re­sis­tance.

In­sulin re­sis­tance may im­prove with weight re­duc­tion and/‍or phar­ma­co­log­ic treat­ment of hy­per­glycemia but is sel­dom re­stored to nor­mal.

The risk of de­vel­op­ing type 2 di­a­betes in­creas­es with age, obe­si­ty, and lack of phys­i­cal ac­tiv­i­ty. It oc­curs more fre­quent­ly in women with prior GDM, in those with hy­per­ten­sion or dys­lipi­demia, and in cer­tain racial/eth­nic sub­groups (African Amer­i­can, Amer­i­can In­di­an, His­pan­ic/‍Latino, and Asian Amer­i­can). It is often as­so­ci­at­ed with a strong ge­net­ic predispo­si­tion or fam­i­ly his­to­ry in first-‍de­gree rel­a­tives, more so than type 1 di­a­betes. How­ev­er, the ge­net­ics of type 2 di­a­betes is poor­ly un­der­stood. In adults with­out tra­di­tion­al risk fac­tors for type 2 di­a­betes and/‍or younger age, con­sid­er an­ti­body test­ing to ex­clude the di­ag­no­sis of type 1 di­a­betes (i.e., GAD).