Administration of human umbilical cord blood to low birth weight infants may prevent the subsequent development of type 2 diabetes
Introduction
A number of epidemiological and experimental studies have shown that impaired intrauterine growth, resulting in low birth weight (less than the 10th percentile), is associated with a variety of adult-onset diseases, including type 2 diabetes, hypertension, hyperlipidemia, cardiovascular disease, stroke [1], [2], [3], [4], [5], [6], [7], [8], [9], [10] and kidney disease [11], [12]. The common underlying mechanism for most of these disease conditions seems to be glucose intolerance and insulin resistance with hyperinsulinemia. Worldwide, maternal malnutrition, leading to poor fetal nutrition, seems to be the important cause of fetal growth retardation [8]. In this under-nourished fetus, it is hypothesized that the nutrient supply to the brain is well preserved at the expense of the other organs. For example, the growth of the pancreas and kidney and possibly the skeletal muscle is reduced. Rats fed a low protein diet during pregnancy results in significant reduction in pancreatic β-cell proliferation and islet cell size in the neonates [13]. In addition, apoptosis of β-cells and decreased islet vascularization was observed in 14-day-old neonates born to low protein diet mothers [14]. Thus, the reduction in β-cell mass occurs at the expense of the growth of the brain. The net result of this “trade off” is a decrease in insulin secretion in the low birth weight infant. Decreased insulin secretion alone is not sufficient to cause glucose intolerance, because the under-nourished infant is usually thin and may have normal insulin sensitivity. However, overfeeding during childhood with development of obesity in adulthood may cause glucose intolerance and insulin resistance, leading to type 2 diabetes later in life [7], [8].
Section snippets
Hypothesis
Lifestyle modification with diet and appropriate caloric intake to improve insulin secretion in the offspring of malnourished pregnant mothers will help prevent the development of type 2 diabetes later in life. However, such a strict lifestyle modification in a growing child is not always feasible. Cherif et al. [15] supplemented pregnant rats on low protein diet with taurine, which stimulates the release of insulin from islet cells, and found restoration of insulin release from malnourished
References (53)
- et al.
Stem-cell therapy for diabetes mellitus
Lancet
(2004) - et al.
Effect of human umbilical cord blood cells on glycemia and insulitis in type 1 diabetic mice
Biochem Biophys Res Commun
(2004) - et al.
Transplantation of human umbilical cord blood cells improves glycemia and glomerular hypertrophy in type 2 diabetic mice
Biochem Biophys Res Commun
(2004) - et al.
Effect of human cord blood transfer on survival and disease activity in MRL-Lpr/Lpr mice
Clin Immunol Immunopath
(1995) - et al.
Stem cells from bone marrow, umbilical cord blood and peripheral blood for clinical application: current status and future application
Crit Rev Oncol Hematol
(1996) - et al.
Administration of human umbilical cord blood cells delays the onset of prostate cancer and increases the lifespan of the TRAMP mouse
Cancer Lett
(2006) The fetal and infant origins of adult disease
BMJ
(1990)Fetal growth and adult disease
Br J Obstet Gynaecol
(1992)- et al.
Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis
Diabetologia
(1992) - et al.
Insulin resistance in short children with intrauterine growth retardation
J Clin Endocrinol Metab
(1997)