Adipokine Profile in Patients with Type 2 Diabetes Depends on Degree of Obesity

Kocot, Joanna; Dziemidok, Piotr; Kiełczykowska, Małgorzata; Hordyjewska, Anna; Szczęśniak, Grzegorz; Musik, Irena

doi:10.12659/msm.904318

Cited by 32 publications

(31 citation statements)

References 35 publications

(59 reference statements)

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“…The magnitude of the influence of adiposity on other adipokines in MetS and subsequent T2DM also varies in the literature. Comparison of normal weight, overweight, obese and morbidly obese T2DM patients with metabolically healthy normal weight controls showed a difference in adipokine markers that did not exist in normal weight T2DM subjects, but the difference was exacerbated by being overweight or (morbidly) obese (49). Adiponectin, a commonly measured anti-inflammatory adipokine, has been shown to be lower in obese subjects compared to metabolically healthy normal weight controls, but there was no difference between obese subjects and T2DM patients (50).…”

Section: Discussionmentioning

confidence: 92%

Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis

Pearsey

Henson

Sargeant

et al. 2020

Rev Endocr Metab Disord

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To systematically review the current literature investigating associations between zinc-alpha2-glycoprotein (ZAG) and dysglycaemia (including type 2 diabetes (T2DM), poly-cystic-ovary syndrome (PCOS), pre-diabetes or insulin resistance). This included relationships between ZAG and continuous measures of insulin and glucose. Additionally, we performed a meta-analysis to estimate the extent that ZAG differs between individuals with or without dysglycaemia; whilst examining the potential influence of adiposity. A systematic search was performed on four databases for studies on circulating ZAG concentrations in adult human populations, comparing healthy controls to individuals with dysglycaemia. Key characteristics, including the mean ZAG concentrations (mg∙L−1), and any correlational statistics between ZAG and continuous measures of glucose, glycated haemoglobin (HbA1c) or insulin were extracted. Meta-analyses were performed to compare metabolically healthy controls to cases, and on studies that compared controls and cases considered overweight or obese (body mass index (BMI) ≥25 kg.m2). 1575 papers were identified and 14 studies (16 cohorts) were considered eligible for inclusion. Circulating ZAG was lower in individuals with dysglycaemia compared to metabolically healthy controls (−4.14 [−8.17, −0.11] mg.L−1; I2 = 98.5%; p < 0.001). When using data from only studies with overweight or obese groups with or without dysglycaemia (three studies (four cohorts); pooled n = 332), the difference in circulating ZAG was no longer significant (−0.30 [−3.67, 3.07] mg. L−1; I2 = 28.0%; p = 0.225). These data suggest that ZAG may be implicated in dysglycaemia, although there was significant heterogeneity across different studies and the mediating effect of adiposity cannot be excluded. Therefore, more research is needed before robust conclusions can be drawn.

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Section: Discussionmentioning

confidence: 92%

Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis

Pearsey

Henson

Sargeant

et al. 2020

Rev Endocr Metab Disord

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show abstract

“…The finding of this study, that a functional analysis of the subnetworks encompassing HOMA-β-associated GWAS signal-harboring genes enriched pathways of especially fat metabolism, with a central role of adipose tissues, support the "lipotoxicity" theory of beta cell failure in T2D, where heightened free fatty acid flux results from adipose tissue leads to increased insulin resistance. Indeed, several studies have demonstrated that obese type 2 diabetic patients presented a disturbed adipokine profile, which seems to be an important link between adiposity (i.e., insulin resistance), beta cell dysfunction, and T2D [29,30]. There is pharmacological evidence that drugs like insulin and thiazolidinediones significantly suppress the free fatty acid flux and improves beta cell functions in diabetes.…”

Section: Discussionmentioning

confidence: 99%

Functional Interactomes of Genes Showing Association with Type-2 Diabetes and Its Intermediate Phenotypic Traits Point towards Adipo-Centric Mechanisms in Its Pathophysiology

Saxena

Wahi²,

Kumar

et al. 2020

Biomolecules

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The pathogenic mechanisms causing type 2 diabetes (T2D) are still poorly understood; a greater awareness of its causation can lead to the development of newer and better antidiabetic drugs. In this study, we used a network-based approach to assess the cellular processes associated with protein–protein interaction subnetworks of glycemic traits—HOMA-β and HOMA-IR. Their subnetworks were further analyzed in terms of their overlap with the differentially expressed genes (DEGs) in pancreatic, muscle, and adipose tissue in diabetics. We found several DEGs in these tissues showing an overlap with the HOMA-β subnetwork, suggesting a role of these tissues in β-cell failure. Many genes in the HOMA-IR subnetwork too showed an overlap with the HOMA-β subnetwork. For understanding the functional theme of these subnetworks, a pathway-to-pathway complementary network analysis was done, which identified various adipose biology-related pathways, containing genes involved in both insulin secretion and action. In conclusion, network analysis of genes showing an association between T2D and its intermediate phenotypic traits suggests their potential role in beta cell failure. These genes enriched the adipo-centric pathways and were expressed in both pancreatic and adipose tissue and, therefore, might be one of the potential targets for future antidiabetic treatment.

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“…также показали достоверные различия уровней резистина у пациентов с ожирением и здоровых людей, однако значимую связь резистина с гликемией натощак и другими метаболическими показателями им удалось выявить только у здоровых лиц [18]. Другие авторы также не выявили корреляции уровня резистина ни с ИМТ у больных с избыточной массой тела [19,20], ни с наличием СД 2 типа [21].…”

Section: Discussionunclassified