Amylin and Its Relation to Insulin and Lipids in Obese Children Before and After Weight Loss*

Vestische Hospital for Children and Adolescents Datteln, University of Witten/Herdecke, Dr. F. Steiner Str. 5, 45711 Datteln, Germany.
Obesity (Impact Factor: 3.73). 09/2007; 15(8):2006-11. DOI: 10.1038/oby.2007.239
Source: PubMed


There are limited data concerning the relationships between amylin, weight status, lipids, insulin, and insulin resistance in obese humans. Therefore, the aim was to study these relationships in cross-sectional and longitudinal analyses.
Fasting amylin, insulin, glucose, triglycerides, low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol, and percentage body fat based on skinfold measurements were determined in 37 obese children (median age, 11.5 years) and compared with 16 lean children of the same age and gender. Furthermore, we analyzed the changes of these variables in the obese children after participating in a one-year weight loss intervention program.
Obese children had significantly (p < 0.01) higher amylin, triglycerides, LDL-cholesterol, and insulin levels as compared with the lean children. In multiple linear regression analysis, amylin was significantly (p < 0.05) correlated to insulin and triglycerides, but not to age, gender, pubertal stage, or BMI. Changes of amylin correlated significantly (p < 0.001) to changes of insulin (r = 0.54) and triglycerides (r = 0.49), but not to changes of BMI or percentage body fat. Substantial weight loss in 17 children led to a significant (p < 0.05) decrease of amylin, triglycerides, and insulin, in contrast to the 20 children without substantial weight loss.
Amylin levels were related to insulin concentrations in both cross-sectional and longitudinal analyses, suggesting a relationship between amylin and insulin secretion. Amylin levels were reversibly increased in obesity and related to triglyceride concentrations.

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    • "Infusion of amylin in dogs also induced peripheral insulin resistance (Xinwei et al., 2011). High levels of amylin are observed in obese children and obese adults with impaired glucose tolerance or type-2 diabetes (Reinehr et al., 2007). Cellular and animal studies implicate multiple roles of amylin in regulating insulin action and glucose and lipid metabolism. "
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    ABSTRACT: The objective of this study was to assess the correlations of amylin (a pancreatic polypeptide hormone) with some hormonal, biochemical and bone parameters in pullets. Forty 18-week-old pullets were used. Plasma amylin, CT (calcitonin), 1,25 (OH)2 vitamin D (1,25 dihydroxycholecalciferol ), serum osteocalcin, glucose, ALP (alkaline phosphatase), cholesterol, and triglycerides, as well as weight, length and total volume of tibiotarsi were measured. Plasma amylin concentration was negatively correlated with serum cholesterol (p<0.05) and triglycerides (p<0.05) concentrations. Plasma amylin concentration was significantly and positively correlated with plasma calcitonin concentrations (p<0.001). Serum ALP and plasma amylin concentrations were positively correlated (p<0.01). There were no correlations between amylin hormone and other parameters. Based on these results, it is possible to conclude that endogen amylin may effect cholesterol, triglycerides, calcitonin, and ALP levels in pullets without changing some other hormonal, biochemical and bone parameters related to calcium and lipid metabolism.
    Revista Brasileira de Ciência Avícola 01/2014; 16(4):375-380. DOI:10.1590/1516-635X1604375-380 · 0.43 Impact Factor
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    • "Plasma amylin levels have been reported to be elevated under pathological conditions which contribute to the development of type 2 diabetes. Elevated circulating levels of amylin have been detected in obese subjects, insulin resistance and type 2 diabetes patients [8]–[11]. Pancreatic amylin mRNA and plasma amylin levels are also elevated in genetically obese, insulin-resistant rats [12]. "
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    ABSTRACT: Amylin is the most abundant component of islet amyloid implicated in the development of type 2 diabetes. Plasma amylin levels are elevated in individuals with obesity and insulin resistance. Monocyte chemoattractant protein-1 (MCP-1, CCL2) is involved in insulin resistance of obesity and type 2 diabetes. We investigated the effect of MCP-1 on amylin expression and the underlying mechanisms with murine pancreatic β-cell line MIN6 and pancreatic islets. We found that MCP-1 induced amylin expression at transcriptional level and increased proamylin and intermediate forms of amylin at protein level in MIN6 cells and islets. However, MCP-1 had no effect on the expressions of proinsulin 1 and 2, as well as prohormone convertase (PC) 1/3 and PC2, suggesting that MCP-1 specifically induces amylin expression in β-cells. Mechanistic studies showed that although there is no detectable CCR2 mRNA in MIN6 cells and islets, pretreatment of MIN6 cells with pertussis toxin inhibited MCP-1 induced amylin expression, suggesting that alternative Gi-coupled receptor(s) mediates the inductive effect of MCP-1. MCP-1 rapidly induced ERK1/2 and JNK phosphorylation. Inhibitors for MEK1/2 (PD98059), JNK (SP600125) or AP1 (curcumin) significantly inhibited MCP-1-induced amylin mRNA expression. MCP-1 failed to induce amylin expression in pancreatic islets isolated from Fos knockout mice. EMSA showed that JNK and ERK1/2 were involved in MCP-1-induced AP1 activation. These results suggest that MCP-1 induces murine amylin expression through AP1 activation mediated by ERK1/2 or JNK. Further studies showed that treatment of MIN6 cells with NF-κB inhibitor or overexpression of IκBα dominant-negative construct in MIN6 cells significantly inhibited MCP-1-induced amylin expression, suggesting that NF-κB related signaling also participates in MCP-1-induced murine amylin expression. MCP-1 induces amylin expression through ERK1/2/JNK-AP1 and NF-κB related signaling pathways independent of CCR2. Amylin upregulation by MCP-1 may contribute to elevation of plasma amylin in obesity and insulin resistance.
    PLoS ONE 05/2011; 6(5):e19559. DOI:10.1371/journal.pone.0019559 · 3.23 Impact Factor
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    • "Insulin resistance is a common feature of childhood obesity. Elevated insulin levels due to insulin resistance might be associated with an increase in amylin concentrations in childhood obesity.17 The results of this study showed that fasting amylin levels were correlated with HOMA-IR in both groups (Fig. 4). "
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    ABSTRACT: Amylin secretion is increased parallel to insulin in obese subjects. Despite their marked obesity, a state of relative hypoinsulinemia occurs in children with Prader-Willi syndrome (PWS). Based on the hypothesis that amylin levels may be relatively low in PWS children, contributing to their excessive appetite, we studied amylin levels after oral glucose loading in children with PWS and overweight controls. Plasma levels of amylin, glucagon, insulin, and glucose were measured at 0, 30, 60, 90, and 120 min after a glucose challenge in children with PWS (n = 18) and overweight controls (n = 25); the relationships among the variables were investigated in these two groups. Amylin levels were significantly correlated with insulin during fasting and during the oral glucose tolerance test in both groups. Amylin levels between 0 and 60 min after glucose loading were statistically different between the two groups. They were lower in children with PWS than in the controls between 0 and 30 min after glucose loading. The relatively low levels of amylin, compared to those in overweight controls, during the early phase of glucose loading in patients with PWS, may contribute, in part, to the excessive appetite of PWS patients as compared to the overweight controls.
    Yonsei medical journal 03/2011; 52(2):257-62. DOI:10.3349/ymj.2011.52.2.257 · 1.29 Impact Factor
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