Non‐catch‐up growth in intrauterine growth‐retarded rats showed glucose intolerance and increased expression of PDX‐1 mRNA

Abstract

Children born with intrauterine growth retardation (IUGR) show long-term complications like non-catch-up growth and type 2 diabetes. We hypothesize that the duration of malnutrition influences the growth and pancreatic development in IUGR. The pancreatic duodenal homeobox-1 (PDX-1) expression might also be different because it links glucose metabolism to the regulation of insulin gene transcription in the pancreas. We made an IUGR rat model with a low-protein diet (8% casein) during gestational periods. Catch-up rats (CU) were given normal lab chow immediately after birth. Non-catch-up rats (NCU) were given normal lab chow after lactation periods. PDX-1 mRNA level, islet areas and intravenous glucose tolerance test (IVGTT) were assessed in each group and compared with control rats (C) at the 16th week. The weight and length of CU and C rats were not different after 3 weeks, while NCU rats were smaller than C and CU rats (P < 0.05). In IVGTT, the 20-min and 50-min glucose level and area under the curve for glucose were increased in NCU rats compared with those values in C and CU rats (P < 0.05). The islet area of NCU rats was smaller than that of C and CU rats (P < 0.05). In contrast, PDX-1 mRNA levels of NCU rats were higher than those of C rats (P < 0.05). CU rats showed normal glucose response in IVGTT with increased islet number and size. IUGR rats that failed to undergo catch-up growth might be prone to abnormal glucose tolerance, decreased islet size, and increased PDX-1 mRNA levels in early adult life.