Adiponectin levels and waist circumference, waist-hip ratio and conicity index in type 1 diabetes patients

Marques, Carlo Aldrovandi Torreão; Beretta, Mileni Vanti; Prates, Raquel Eccel; Nascimento, Filipe; Nascimento, Cigléa do; Almeida, Juliano Milanezi de; Rodrigues, Ticiana da Costa

doi:10.1186/1758-5996-7-s1-a86

Cited by 3 publications

(2 citation statements)

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“…It has been previously shown that the relationship that this adipokine has with both insulin sensitivity in adipose tissue and uric acid secretion. 44, 31, 45 Our results suggest that adiponectin acts as a significant mediator inside our proposed mediation model, which confirms that the endocrinometabolic regulation arising from VAT is partially responsible for the role uric acid plays inside this relationship, as pictured in Figure 7.3b and previously proven in an in vitro environment. 20…”

Section: Discussionsupporting

confidence: 86%

Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

Fernández‐Chirino

Antonio-Villa

Vargas‐Vázquez

et al. 2020

Preprint

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BACKGROUND: Serum uric acid (SUA) has a relationship with cardiometabolic conditions such as insulin resistance (IR) and visceral adipose tissue (VAT) accumulation. Here, we aimed to clarify the nature of this relationship and the underlying causality mechanism. METHODS: We conducted a population-based cross-sectional study comprising 8,504 subjects joining both NHANES 2003-2004 and 2011-2012 cycles and ENSANUT Medio Camino 2016. We performed mixed effects linear regression models using HOMA2-IR, adipoIR, and METS-VF as indicators of IR and VAT accumulation. Furthermore, we performed mediation analyses to assess a potential causal mechanism and ROC curves to establish cut-off points for identification of IR and visceral obesity using SUA. Finally, with an additional dataset comprised of 226 subjects with both euglycemic hyperinsulinemic clamp (EHC) and dual X-ray absorptiometry (DXA) measurements for IR and VAT accumulation, we performed a network of confirmatory mediation analyses. RESULTS:We found that SUA has a mediating role inside the bidirectional relationship between IR and visceral obesity, and it is part of an underlying causality mechanism which includes adiponectin. The proportion of the mechanism mediated by SUA is greater when stated that IR (in either peripheral or adipose tissue) leads to VAT accumulation (14.90%[13.20%-17.00%] and 15.54%[13.61% - 18.00%] to 4.88%[3.06%-7.00%] and 8.13%[5.91% - 10.00%]) instead of the opposite direction. This result was confirmed by mediation analyses using gold-standard measurements. CONCLUSIONS:Elevated SUA acts as mediator inside the bidirectional relationship between IR andVAT accumulation. Its role appears to be larger when considering adipose tissue IR as the promoter for VAT accumulation.

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Section: Discussionsupporting

confidence: 86%

Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

Fernández‐Chirino

Antonio-Villa

Vargas‐Vázquez

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Body fat distribution affects serum adiponectin levels. One limitation of this report was the lack of any measurement that reflects body fat distribution, such as waist-hip [50] or visceral fat ratios [51]. Another limitation was our failure to collect information on the eating behavior of the participants, such as skipping breakfast or eating slowly.…”

Section: Discussionmentioning

confidence: 99%

Single nucleotide polymorphism in the ADIPOQ gene modifies adiponectin levels and glycemic control in type two diabetes mellitus patients

Al¹,

Alfaqih²,

Alorjani³

2022

EJEA

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Diabetes mellitus (DM) is the ninth leading cause of death worldwide. Mortality from DM is largely attributed to disease complications. Glycemic control of DM patients reduces mortality. Studies indicated that the lack of glycemic control in DM patients could be influenced by the genetic background of the patients. Evidence suggests that adiponectin levels are dysregulated in DM patients with poor glycemic control. Serum adiponectin level is a heritable trait influenced by single nucleotide polymorphisms (SNPs) in the ADIPOQ gene. It is hypothesized that SNPs in ADIPOQ could modify glycemic control in DM patients. To test this hypothesis, 375 type 2 DM (T2DM) patients were recruited. Patients were classified into good vs. poor glycemic control according to hemoglobin A1c levels. Study subjects were genotyped for variations of four SNPs in ADIPOQ (rs17300539, rs266729, rs2241766, and rs1501299). Adiponectin levels were measured from the serum. Our analysis showed that reduced serum adiponectin, a longer duration of treatment, and increased insulin resistance were all significant predictors of poor glycemic control. Moreover, the T allele and the TT genotype of rs2241766 were significantly more frequent in patients with poor glycemic control (P < 0:05). Individuals with the TT genotype of rs2241766 had significantly lower levels of serum adiponectin (P < 0:05). It was concluded that lower levels of serum adiponectin and the T allele of rs2241766 SNP in ADIPOQ were associated with poor glycemic control in T2DM patients.

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Single Nucleotide Polymorphism in the ADIPOQ Gene Modifies Adiponectin Levels and Glycemic Control in Type Two Diabetes Mellitus Patients

Alfaqih

Al-Hawamdeh

Amarin

et al. 2022

BioMed Research International

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Diabetes mellitus (DM) is the ninth leading cause of death worldwide. Mortality from DM is largely attributed to disease complications. Glycemic control of DM patients reduces mortality. Studies indicated that the lack of glycemic control in DM patients could be influenced by the genetic background of the patients. Evidence suggests that adiponectin levels are dysregulated in DM patients with poor glycemic control. Serum adiponectin level is a heritable trait influenced by single nucleotide polymorphisms (SNPs) in the ADIPOQ gene. It is hypothesized that SNPs in ADIPOQ could modify glycemic control in DM patients. To test this hypothesis, 375 type 2 DM (T2DM) patients were recruited. Patients were classified into good vs. poor glycemic control according to hemoglobin A1c levels. Study subjects were genotyped for variations of four SNPs in ADIPOQ (rs17300539, rs266729, rs2241766, and rs1501299). Adiponectin levels were measured from the serum. Our analysis showed that reduced serum adiponectin, a longer duration of treatment, and increased insulin resistance were all significant predictors of poor glycemic control. Moreover, the T allele and the TT genotype of rs2241766 were significantly more frequent in patients with poor glycemic control ( P < 0.05 ). Individuals with the TT genotype of rs2241766 had significantly lower levels of serum adiponectin ( P < 0.05 ). It was concluded that lower levels of serum adiponectin and the T allele of rs2241766 SNP in ADIPOQ were associated with poor glycemic control in T2DM patients.

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Adiponectin levels and waist circumference, waist-hip ratio and conicity index in type 1 diabetes patients

Cited by 3 publications

References 0 publications

Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

Single nucleotide polymorphism in the ADIPOQ gene modifies adiponectin levels and glycemic control in type two diabetes mellitus patients

Single Nucleotide Polymorphism in the ADIPOQ Gene Modifies Adiponectin Levels and Glycemic Control in Type Two Diabetes Mellitus Patients

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