Altered Plasma Adipokine Levels andin VitroAdipocyte Differentiation in Pediatric Type 1 Diabetes

Abstract

The adipogenic effects of diabetic plasma in vitro and the altered adipokine levels in vivo suggest adipose tissue involvement in the low-grade inflammation associated with T1D, already in pediatric patients.

Effect of High Glucose Levels on White Adipose Cells and Adipokines—Fuel for the Fire

“…Verrijn Stuart et al found that hyperglycaemic plasma from type 1 diabetes patients enhanced the extent of adipocyte differentiation of normal preadipocytes [24]. However, high glucose concentrations alone had no effect of adipogenesis.…”

“…Verrijn Stuart et al found that in type 1 diabetes patients, plasma levels of adiponectin, leptin, retinal binding protein (RBP)-4, cathepsin S, tissue inhibitor of metalloproteinase-1, chemerin, serum amyloid A-1, plasminogen activator inhibitor-1 (PAI)-1, and CCL2 levels were increased compared to control subjects [24]. No significant differences were found in the other plasma adipokines studied, including IL-1RA, IL-1β, IL-6, IL-10, TNF-α, interferon-γ, macrophage inhibitory factor, IL-8, C-X-C motif ligand (CXCL) 10, γ interferon inducible protein 10, granulocyte-macrophage colony stimulating factor, resistin, thrombopoietin, and adipsin.…”

“…In the context of hyperglycaemia arising from type 1 diabetes, Verrijn Stuart et al investigated whether elevations in plasma adipokine levels correlated with rates of adipokine release from adipocytes [24]. They first tested the effect on normal adipocytes incubated with plasma from patients with type 1 diabetes versus controls, and noted higher rates of release of CCL2, TNF-α, adiponectin, as well as upward trends for RBP-4 and cathepsin S. In contrast, high glucose levels alone increased CCL2 secretion and lowered adiponectin and RBP4 by adipocytes, without any changes in cathepsin S, chemerin, leptin, or PAI-1.…”

Chemerin concentration in children with type 1 diabetes

“…Badania nad rolą tej adipocytokiny w patogenezie cukrzycy typu 1 i jej powikłań naczyniowych nie są liczne [12][13][14]. Czy poprzez zaangażowanie tkanki tłuszczowej w patomechanizm obu schorzeń cukrzyca typu 1 i 2 może stanowić swego rodzaju kontinuum?…”

“…Stężenie IFN-γ u pacjentów z cukrzycą typu 1 i w grupie kontrolnej Fig. 3 żenie chemeryny jest istotnie większe zarówno w cukrzycy nowo rozpoznanej, jak i trwającej powyżej roku w porównaniu z grupą kontrolną [12]. Grupa holenderska obejmowała jednak zaledwie dwadzieścioro dzieci z nowo rozpoznaną oraz dwadzieścioro dzieci z dłużej trwającą cukrzycą [12].…”