ðə mˈaʊs mˈɑːdəl ʌv mətʃˈʊɹɹᵻɾiˈɑːnsɛt dˌaɪəbˈiːɾiːz ʌvðə jˈʌŋ mˈoʊdi dˌaɪəbˈiːɾiːz sədʒˈɛstᵻd ðætðə ɹᵻdˈuːst ɡlɪklˈeɪzaɪd klˈɪɹəns stˈændz bᵻhˌaɪnd ðɛɹ θˌɛɹəpjˈuːɾɪk səksˈɛs ɪn hjˈuːmən mˈoʊdi pˈeɪʃənts, bˌʌt ˌɜːbɐnˈoʊvə ˈɛt ˈæl. fˈaʊnd ðæt hjˈuːmən mˈoʊdi pˈeɪʃənts ɹᵻspˈɑːnd dˈɪfɹəntli ænd ðæt ðɛɹwˌʌz nˈoʊ kənsˈɪstənt dˈiːkɹiːs ɪn ɡlɪklˈeɪzaɪd klˈɪɹəns ɪn ɹˈændəmli sᵻlˈɛktᵻd ˌeɪtʃˌɛnˈɛf wˈʌn ˈeɪmˈoʊdi ænd ˌeɪtʃˌɛnˈɛf fˈoːɹ ˈeɪmˈoʊdi pˈeɪʃənts.
The mouse model of Maturity-onset diabetes of the young (MODY) diabetes suggested that the reduced gliclazide clearance stands behind their therapeutic success in human MODY patients, but Urbanova et al. found that human MODY patients respond differently and that there was no consistent decrease in gliclazide clearance in randomly selected HNF1A-MODY and HNF4A-MODY patients.