4.5.0.0 Non­al­co­holic Fatty Liver Dis­ease

Di­a­betes is as­so­ci­at­ed with the de­vel­opment of non­al­co­holic fatty liver dis­ease, in­clud­ing its more se­vere man­i­fes­ta­tions of non­al­co­holic steatohep­ati­tis, liver fibro­sis, cir­rho­sis, and hep­a­to­cel­lu­lar car­ci­no­ma (43). El­e­va­tions of hep­at­ic transam­i­nase con­cen­tra­tions are as­so­ci­at­ed with high­er BMI, waist cir­cum­fer­ence, and triglyc­eride lev­els and lower HDL choles­terol lev­els. Non­in­va­sive tests, such as elas­tog­ra­phy or fibro­sis biomark­ers, may be used to as­sess risk of fibro­sis, but re­fer­ral to a liver spe­cial­ist and liver biop­sy may be re­quired for defini­tive di­ag­no­sis (43a). In­ter­ven­tions that im­prove metabol­ic abnor­malities in pa­tients with di­a­betes (weight loss, glycemic con­trol, and treat­ment with specific drugs for hy­per­glycemia or dys­lipi­demia) are also beneficial for fatty liver dis­ease (44,45). Pi­ogli­ta­zone and vi­ta­min E treat­ment of biop­sy-‍proven non­al­co­holic steatohep­ati­tis have been shown to im­prove liver his­tol­o­gy, but ef­fects on longert­erm clin­i­cal out­comes are not known (46,47). Treat­ment with li­raglu­tide and with sodi­um–glu­cose co­trans­porter 2 in­hibitors (da­pagliflozin and em­pagliflozin) has also shown some promise in pre­lim­i­nary stud­ies, al­though benefits may be me­di­at­ed, at least in part, by weight loss (48–50).