Association between ferritin and hepcidin levels and inflammatory status in patients with type 2 diabetes mellitus and obesity

Andrews, Mónica; Soto, Néstor; Arredondo, Miguel

doi:10.1016/j.nut.2014.04.019

Cited by 69 publications

(70 citation statements)

References 52 publications

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“…And There was significant correlation of expression of TLR2 and TLR4with body mass index (BMI). our results also are consistent with (Andrews, S et al 2015) (17)who revealed increased gene expression of TNF-α, IL-6, NF-κB, and TLR-2/4 in patients with diabetes, obesity, or both exacerbate and perpetuate the insulin resistance and inflammatory state.…”

Section: Discussionsupporting

confidence: 93%

“…Though classically described as receptors for antigens associated with a variety of bacteria, viruses, and fungi, recent reports suggest that TLRs also sense and respond to nutritional fatty acids. In this capacity, TLRs may be viewed as a possible bridge between nutrition and molecular inflammation, the harbinger of metabolic syndrome [15][16][17][18].…”

Section: Discussionmentioning

confidence: 99%

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TLR2 and IL 18 in obese diabetic patient

Mohamed¹,

Abd-Elraheem²,

Nahrery³

et al. 2016

J Diabetes Metab

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Objective: This study was conducted to determine expression ofTLR2 in peripheral blood monocytes and the proinflammatory cytokine IL18 in type 2 diabetic obese patients to explain a possible pathophysiological link between obesity and inflammation leading to insulin resistance. Methodology:This study was conducted in Al-Zahra University Hospital .The study population consisted of 40 patients divided into 3 groups : 15 obese non diabetic patients, 15 diabetic obese patients and 10 normal body weight clinically and laboratory free served as a control group . All studied groups were subjected to clinical examination and laboratory investigations which include lipid profile, fasting blood glucose, Hb A1C, serum insulin, HOMA IR, Serum IL 18 and flow cytometric analysis expression of TLR-2 on CD14+ monocytes.Results: IL-18 levels were significantly higher in obese non diabetic group(61.5 ± 8.2 ng/l) and diabetic obese group (62.8 ± 10.9 ng/l) when compare to normal control group (26.5 ± 6.5 ng/l) (p<0.000) , while there were no significant change between obese non diabetic group and diabetic obese group regarding IL-18 levels (p 0. 713) and there was a highly significant increase in TLR-2 MFI in obese non diabetic group (9.3 + 3.2 ), diabetic obese group (16.7 + 3.4)when compared to controls group (4.5 + 1.2), also levels of TLR-2MFI were significantly higher in obese diabetic group compared to obese non diabetic group (p< 0.001) . There was a significant increase in HOMA-IR in obese non diabetic group (3.81 + 0.97), diabetic obese group (11.55+3.89) when compared to controls group (2.46 + 0.95)(p<0.0025) (P<0.001). Also levels of HOMA IR were significantly higher in obese diabetic group compared to obese non diabetic group (p< 0.00). There was a significant increase in insulin levels in obese non diabetic group (16.4 + 3.72uU/L), diabetic obese group (21.40 + 3.98uU/l) when compared to controls group (11.2 + 2.94 uU/L) (p< 0.008), also levels of insulin were significantly higher in obese non diabetic group compared to obese diabetic group (p< 0.0014). There was a significant positive correlation between TLR2 MFI and each of insulin, IL18 and BMI in obese non diabetic as well as diabetic obese patients. Conclusions:This study demonstrated that the expression of TLR-2 on CD14+ monocytes was up regulated in obese non diabetic and obese diabetic patients and was associated with inflammatory response as assessed by increased serum levels of IL-18.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

TLR2 and IL 18 in obese diabetic patient

Mohamed¹,

Abd-Elraheem²,

Nahrery³

et al. 2016

J Diabetes Metab

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“…or only in obese individuals (38,45,46). We performed an analysis in order to investigate the influence of BMI in cytokine levels.…”

Section: Discussionmentioning

confidence: 99%

IL-6, TNF-α, and IL-10 levels/polymorphisms and their association with type 2 diabetes mellitus and obesity in Brazilian individuals

Rodrigues

Pietrani

Bosco

et al. 2017

Arch. Endocrinol. Metab.

107

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Objective: This study aimed to investigate the association of plasma TNF-α, IL-6, and lL-10 levels and cytokine gene polymorphisms , and IL-10 (-1082 A→G, -819 T→C and -592 A→C)] in type 2 diabetes mellitus (T2DM) and obese patients. Subjects and methods: One hundred and two T2DM patients and 62 controls were included in this study. Cytokine plasma levels were measured by the Cytometric Bead Array method. Genotyping was carried out by the polymerase chain reaction. Results: IL-6 levels were significantly different between T2DM patients and controls. Interestingly, IL-6 levels were higher in T2DM patients with BMI > 30 kg/m 2 compared with other patients and obese controls. The genotype and allele frequencies were similar between patients and controls. In the T2DM group, the SNP IL-10 -819 T/C showed a difference between the cytokine level and genotypes: IL-10 level in the TT genotype was significantly higher when compared to CC genotype. Conclusions: These results suggest an association between IL-6 levels and obesity, and IL-10 levels and the SNP -819 T/C in T2DM. Knowledge of these variants in T2DM might contribute to a better understanding of the role of inflammation in the etiology and progression of this disease.

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“…The expression of genes involved in the immune response, TNF-α, IL-6, NF-kB, and TLR-2/4, in patients with diabetes and obesity alters the metabolism of glucose and fatty acids, increasing oxidative stress and levels of micronutrients such as iron [153]. Thus, elevated serum concentrations of ferritin and hepcidin lead to insulin resistance in type 2 diabetes mellitus due to the sensitization of peripheral glucose receptors.…”

Section: Hepcidinmentioning

confidence: 99%

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

et al. 2017

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Iron is an essential metal for cell survival that is regulated by the peptide hormone hepcidin. However, its influence on certain diseases is directly related to iron metabolism or secondary to underlying diseases. Genetic alterations influence the serum hepcidin concentration, which can lead to an iron overload in tissues, as observed in haemochromatosis, in which serum hepcidin or defective hepcidin synthesis is observed. Another genetic imbalance of iron is iron-refractory anaemia, in which serum concentrations of hepcidin are increased, precluding the flow and efflux of extra- and intracellular iron. During the pathogenesis of certain diseases, the resulting oxidative stress, as well as the increase in inflammatory cytokines, influences the transcription of the HAMP gene to generate a secondary anaemia due to the increase in the serum concentration of hepcidin. To date, there is no available drug to inhibit or enhance hepcidin transcription, mostly due to the cytotoxicity described in the in vitro models. The proposed therapeutic targets are still in the early stages of clinical trials. Some candidates are promising, such as heparin derivatives and minihepcidins. This review describes the main pathways of systemic and genetic regulation of hepcidin, as well as its influence on the disorders related to iron metabolism.

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Association between ferritin and hepcidin levels and inflammatory status in patients with type 2 diabetes mellitus and obesity

Cited by 69 publications

References 52 publications

TLR2 and IL 18 in obese diabetic patient

TLR2 and IL 18 in obese diabetic patient

IL-6, TNF-α, and IL-10 levels/polymorphisms and their association with type 2 diabetes mellitus and obesity in Brazilian individuals

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

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