<p>Abdominal Fat Is Directly Associated With Inflammation In Persons With Type-2 Diabetes Regardless Of Glycemic Control – A Jordanian Study</p>

Abstract

Background and aim: Systemic inflammation is related to the progression of complications associated with diabetes. This study aimed to investigate the association between general and abdominal obesity and inflammation in patients with type-2 diabetes with or without glycemic control. Methods: A total of 198 men (n=73) and women (n=125) diagnosed with type 2 diabetes participated in this study. General obesity markers, body mass index (BMI), and abdominal fat were assessed. Circulating concentrations of glycated hemoglobin (HbA1C), C-reactive protein (CRP), and serum interleukin-6 (IL-6) were determined. Poor glycemic control and good glycemic control were defined as having fasting HbA1C concentrations ≥7% and <7%, respectively. Multivariate adjusted analysis of covariance was used to determine the relation between BMI and abdominal fat and markers of inflammation in patients with good and poor glycemic control. Results: Patients in <7% HbA1C category, those with high abdominal fat had ≈262% higher CRP and ≈30.6% higher IL-6 compared to those with low abdominal fat (p˂0.05). Patients in ≥7% HbA1C category, those with high abdominal fat had ≈41.4% higher CRP and ≈33.9%higher IL-6 compared to those with low abdominal fat (p˂0.05). Abdominal fat was directly related to CRP (p˂0.023) and IL-6 (p˂0.002) concentrations in both groups of type-2 diabetic patients with <7% and ≥7% HbA1C. In patients with ≥7% HbA1C, BMI was directly related to CRP (p˂0.02) and IL-6 (p˂0.047). Whereas in patients with <7% HbA1C, BMI was not associated with CRP or IL-6 concentrations. Conclusion: High level of abdominal fat is associated with systemic inflammation in type-2 diabetes regardless of glycemic control. Abdominal fat is a better predictor (determinant) of inflammation than BMI in patients with type-2 diabetes with or without glycemic control.

The Relation between Eating Habits and Abdominal Fat, Anthropometry, PON1 and IL-6 Levels in Patients with Multiple Sclerosis

“…Regarding the relation to anthropometric variables, there is a positive correlation with WHtR and waist circumference, while this did not happen with fat percentage, WHR, hip circumference and BMI. It seems to indicate that IL-6 is positively associated with fat accumulated in the abdominal area, as observed by other authors [10]. This is verified with significantly higher levels of interleukin in patients with this kind of obesity, which is also linked to the inflammatory status of the disease [5].…”

“…Amongst the cytokines related to MS, interleukin 6 (IL-6) takes the spotlight, due to its high levels in blood serum in MS patients [7] and the fact that it is related to the pathogenesis of the disease [8]. In addition, IL-6 is positively correlated with obesity [9], and especially with an increase in abdominal fat [10]. These metabolic alterations have an influence on oxidation state, modifying biochemical markers that are also related to inflammation, such as the enzyme paraoxonase 1 (PON1).…”

[Retracted] Sex Differences in the Relationship between Abdominal Obesity and Cardiovascular Death in Elderly Patients with Permanent Pacemakers Implantation: A Retrospective Cohort Study

“…Although the mechanism underlying the association between WC and cardiovascular death has not been elucidated, several factors can explain this phenomenon. First, compared to fat stored in other parts of the body, abdominal fat greatly afects infammation [27]. Further, recently, infammatory markers such as C-reactive protein have been reported to be associated with cardiovascular mortality [28].…”

<p>Association Metabolic Obesity Phenotypes with Cardiometabolic Index, Atherogenic Index of Plasma and Novel Anthropometric Indices: A Link of FTO-rs9939609 Polymorphism</p>

“…3,4 In obese individuals, the extra fat tissue causes low-grade chronic inflammation. 5 The adipocytes produce adipocytokines such as TNFα and IL-6. 6 During low-grade systemic inflammation, the insulin-dependent tissues are exposed to infiltration of inflammatory macrophages which effect on tissues performance in response to insulin.…”