Adiponectin Is Present in Cord Blood but Is Unrelated to Birth Weight

Abstract

OBJECTIVE -In adults, adiponectin is reduced in association with excess adiposity, type 2 diabetes, and hyperinsulinemia. We assessed whether adiponectin was 1) present in the fetal circulation, 2) altered in the fetal circulation in the presence of maternal diabetes, and 3) had relations to fetal cord blood insulin or adiposity.RESEARCH DESIGN AND METHODS -We assessed adiponectin in cord blood in a large cohort of singleton offspring of diabetic mothers (ODM; n ϭ 134) and control mothers (n ϭ 45).RESULTS -Adiponectin was present in cord blood and, in ODM, was higher in those delivered at later gestational ages (Spearman r ϭ 0.18, P ϭ 0.03). Adiponectin was slightly lower in ODM than control subjects (ODM 19.7 Ϯ 6.1 vs. control 21.8 Ϯ 5.3 g/ml; P ϭ 0.04), although this difference could potentially reflect different gestational ages in the two groups (ODM 37.6 Ϯ 1.5 and control 40.1 Ϯ 1.1 weeks). In contrast to adults, adiponectin levels in the fetus were unrelated to the degree of adiposity, blood insulin, or leptin in either control subjects or ODM.CONCLUSIONS -Adiponectin is present in cord blood but does not show expected physiological relations with adiposity as observed in adults. Diabetes Care 26:2244 -2249, 2003A dipose tissue expresses a variety of secretory proteins of importance to metabolic and vascular disease. Recently, adiponectin, a 244 -amino acid adipocyte-derived protein (1) has been described that is paradoxically reduced in obesity (2) and inversely related to leptin concentrations (3), despite being solely derived from adipose tissue in humans. Both type 2 diabetes and relative insulin resistance (in nondiabetic subjects) are associated with decreased adiponectin concentrations (4,5), while improvement of insulin sensitivity by either weight reduction (6) or administration of thiazolidinediones (7) is associated with increased adiponectin concentrations. Furthermore, in people matched for BMI, higher adiponectin concentrations are protective against later development of type 2 diabetes (8).Exposure to maternal diabetes in utero is associated with increased adiposity at birth (9), as well as increases in fetal leptin (10) and insulin (11). Furthermore, the presence of maternal diabetes during pregnancy influences the longterm health of offspring with increases in future risk of obesity (12,13), type 2 diabetes (14), and impaired glucose tolerance (15-17).Adiponectin has not been previously assessed in cord blood specimens. We wished to examine whether 1) adiponectin was present in cord blood, 2) relations to adiposity, sex, and circulating insulin and leptin observed in adults were also present in utero, and 3) offspring of mothers with type 1 diabetes, a group at high risk of later development of metabolic disease, would have lower concentrations of adiponectin at birth. RESEARCH DESIGN AND METHODS Recruitment and clinical protocolRecruitment, which began in January 1999 and ended in May 2001, took place in eight hospital-based antenatal centers in Scotland. A total of 250 women with type 1 ...

Relation between fetal anthropometric parameters and cord blood adiponectin and high-sensitivity C-reactive protein in gestational diabetes mellitus

“…In contrast, Lindsay and cols. (9) found no significant correlation between adiponectin concentration and anthropometric parameters. Another study suggested a reverse correlation between PI and adiponectin concentration (11,25).…”

“…Studies have shown that adiponectin affects insulin sensitivity, β oxidation and inflammatory pathways. The fact that adiponectin concentrations increase at later gestational ages suggests a role for it in the early growth and development of the fetus (9,13). The present study revealed that the mean cord blood adiponectin concentration in the GDM group was significantly higher than that in the NGT group.…”

“…Genes for lipid metabolism and those for inflammatory pathways are upregulated in the placenta of women with GDM (2). This upregulation increases or unbalances production of inflammatory cytokines and energy metabolism regulatory cytokines such as adipokines (2,6,7), which increases adiposity at birth (8,9) and predisposes the newborn to become overweight and develop metabolic diseases such as impaired glucose tolerance, metabolic syndrome, and cardiovascular disease (2,(6)(7)(8). Previous studies have focused on the pathophysiologic pathways and cytokine levels in GDM and their possible effect on offspring comorbidities later in life (1,6,7,10).…”

“…The origin of adiponectin in the fetus is not clearly understood (13). In adults, adiponectin concentration is inversely related to adiposity, but its association with adiposity is poorly understood (9,11,13). Some studies indicate a positive correlation between cord plasma adiponectin concentration and adiposity in infants (8,12,14,(16)(17)(18)(19)(20) and some have found no significant correlation (9,15).…”

Association of adiponectin polymorphism with cord blood adiponectin concentrations and intrauterine growth

“…11 Although adiponectin levels in the cord blood of term infants are extensively higher than in children or adults, its exact physiological role in regulating intrauterine fetal growth has not been fully elucidated. 8,9,12 On the other hand, epidemiological studies have revealed that there is a relationship between fetal growth retardation and the subsequent development of insulin resistance later in life. 13,14 Single-nucleotide polymorphisms (SNPs) in the adiponectin gene (ADIPOQ) have been associated with adiponectin levels, changes in insulin sensitivity and risk for type 2 diabetes mellitus and coronary artery disease.…”