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

Abstract

BACKGROUND: 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.

METHODS: 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.

RESULTS: 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.

CONCLUSIONS: 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.