Type 2 Diabetes With Non-alcoholic Fatty Liver (NAFLD) Clinical Trial
In this study, the investigators investigate beneficial effects of ipragliflozin, newly developted SGLT2 inhibitor, on reduction in visceral fat area and degree of fatty liver in subjects with T2DM when added to metformin and pioglitazone therapy.
Pioglitazone, a peroxisome proliferator-activated receptor-γ (PPARγ) agonist increase
insulin sensitivity in peripheral tissue and liver by protecting non-adipose tissues against
excessive lipid overload and by balancing the secretion of adipocytokines.
However, PPARγ is a key transcription factor that induces the differentiation adipocyte
maturation and stimulates the induction of enzymes involved in lipogenesis. As a result, the
effect of pioglitazone is generally accompanied by weight gain and an increase in amount of
subcutaneous fat.
Obesity would coexist with fatty liver disease and both conditions aggravate hyperglycemia
in diabetes. According to recent study, up-regulated PPARγ expression in liver was reported
in obesity with hepatic steatosis which implies pioglitazone might induce fatty liver
disease.
A novel oral antidiabetic drug, sodium glucose cotransporter 2 (SGLT2) inhibitor reduces
renal glucose reabsorption and increasing renal glucose excretion thereby promoting energy
loss. As a result, it prevents weight gain and fluid retention which might counteract the
unfavorable effects of pioglitazone treatment.
No study has been conducted on the additional effect on obesity and fatty liver of
ipragliflozin in T2DM patients treated with pioglitazone and metformin.
In this study, the investigators investigate beneficial effects of ipragliflozin, newly
developted SGLT2 inhibitor, on reduction in visceral fat area and degree of fatty liver in
subjects with T2DM when added to metformin and pioglitazone therapy.
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