Association of lipid profile test values, type-2 diabetes mellitus, and periodontitis

Kalsi, DS; Chopra, Jyoti; Sood, Anchal

doi:10.4103/0975-962x.157270

Cited by 11 publications

(7 citation statements)

References 25 publications

(23 reference statements)

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“…1 Several risk factors have been associated with the onset of T2DM, including family history, ethnicity, obesity, and abnormal serum lipid levels. [6][7][8] Low-grade inflammation 9,10 and innate immune response have been implicated as important pathogenic determinants of DM and late diabetic complications. [11][12][13] Among innate immune receptors, Toll-like receptor 4 (TLR4) is one of the key receptors forming an initial line of defense.…”

Section: Introductionmentioning

confidence: 99%

<p>TLR4 Polymorphisms (896A>G and 1196C>T) Affect the Predisposition to Diabetic Nephropathy in Type 2 Diabetes Mellitus</p>

Khaghanzadeh¹,

Naderi²,

Pournasrollah³

et al. 2020

DMSO

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Purpose: Type 2 diabetes mellitus (T2DM) is a disease with a steadily increasing incidence throughout the world. Some molecules regulating the innate immune responses such as tolllike receptor 4 (TLR4) have shown to be involved in late diabetic complications. This study aimed to investigate the association of TLR4 gene polymorphisms with clinicopathological aspects of T2DM in the Iranian population. Patients and Methods: Two TLR4 896A>G and 1196C>T polymorphisms were assessed in 100 T2DM patients and 100 healthy controls using sequence-specific primers PCR. Demographic, anthropometric, and biochemical parameters were obtained from the participants. Results: After logistic regression, in 1196C>T, a significant association was shown between diabetic nephropathy (DN) and CT genotype (P= 0.04, OR= 4.35, CI= (1.04-18.1)). TG level has increased significantly in both T2DM and control subjects with CT genotype (P= 0.027, OR= 1.005, 95% CI= (1.001-1.01)). For 896A>G variant, a significant association was also detected between AG genotype and increased oral glucose tolerance test (OGTT) level (P= 0.048, OR= 1.003, 95% CI= (1.00-1.005)). Conclusion: Although minor alleles of 1196C>T and 896A>G variants have not directly been associated with type 2 diabetes, by involving in the dysregulation of serum TG and blood sugar levels, they might increase the risk of DN.

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Section: Introductionmentioning

confidence: 99%

<p>TLR4 Polymorphisms (896A>G and 1196C>T) Affect the Predisposition to Diabetic Nephropathy in Type 2 Diabetes Mellitus</p>

Khaghanzadeh¹,

Naderi²,

Pournasrollah³

et al. 2020

DMSO

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show abstract

“…Lipid and glucose metabolism disorders are the main characteristics of insulin-resistant type 2 diabetes mellitus [ 1 ]; these disorders are also the basic pathology in diabetic microvascular complications [ 2 ]. Stable glucose-lowering and lipid-lowering therapies effectively retard the progression of chronic diabetic microvascular complications [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Polydatin ameliorates lipid and glucose metabolism in type 2 diabetes mellitus by downregulating proprotein convertase subtilisin/kexin type 9 (PCSK9)

Wang

et al. 2016

Cardiovasc Diabetol

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BackgroundAbnormalities in lipid and glucose metabolism are constantly observed in type 2 diabetes. However, these abnormalities can be ameliorated by polydatin. Considering the important role of proprotein convertase subtilisin/kexin type 9 (PCSK9) in metabolic diseases, we explore the possible mechanism of polydatin on lipid and glucose metabolism through its effects on PCSK9.MethodsAn insulin-resistant HepG2 cell model induced by palmitic acid (PA) and a db/db mice model were used to clarify the role of polydatin on lipid and glucose metabolism.ResultsIn insulin-resistant HepG2 cells, polydatin upregulated the protein levels of LDLR and GCK but repressed PCSK9 protein expression, besides, polydatin also inhibited the combination between PCSK9 and LDLR. Knockdown and overexpression experiments indicated that polydatin regulated LDLR and GCK expressions through PCSK9. In the db/db mice model, we found that polydatin markedly enhanced GCK and LDLR protein levels, and inhibited PCSK9 expression in the liver. Molecular docking assay was further performed to analyze the possible binding mode between polydatin and the PCSK9 crystal structure (PDB code: 2p4e), which indicated that steady hydrogen bonds formed between polydatin and PCSK9.ConclusionsOur study indicates that polydatin ameliorates lipid and glucose metabolism in type 2 diabetes mellitus by downregulating PCSK9.

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“…T2DM is a metabolic disorder characterized by insulin resistance (IR) and pancreatic β-cells dysfunction as a consequence of unsettled hyperglycemia ( Butler et al, 2003 ). Glucose and lipid metabolism disorders are the main characteristics of insulin-resistant type2 diabetes mellitus ( Kalsi et al, 2015 ). These disorders are also the basic pathology in diabetic microvascular complication ( Stratton et al, 2000 ).…”

Section: Introductionmentioning

confidence: 99%

Paeonol Ameliorates Glucose and Lipid Metabolism in Experimental Diabetes by Activating Akt

Xiao

Liu

et al. 2019

Front. Pharmacol.

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Our previous study proved that paeonol (Pae) could lower blood glucose levels of diabetic mice. There are also a few reports of its potential use for diabetes treatment. However, the role of Pae in regulating glucose and lipid metabolism in diabetes remains largely unknown. Considering the critical role of serine/threonine kinase B (Akt) in glucose and lipid metabolism, we explored whether Pae could improve glucose and lipid metabolism disorders via Akt. Here, we found that Pae attenuated fasting blood glucose, glycosylated serum protein, serum cholesterol and triglyceride (TG), hepatic glycogen, cholesterol and TG in diabetic mice. Moreover, Pae enhanced glucokinase (GCK) and low-density lipoprotein receptor (LDLR) protein expressions, and increased the phosphorylation of Akt. In insulin-resistant HepG2 cells, Pae increased glucose uptake and decreased lipid accumulation. What’s more, Pae elevated LDLR and GCK expressions as well as Akt phosphorylation, which was consistent with the in vivo results. Knockdown and inhibition experiments of Akt revealed that Pae regulated LDLR and GCK expressions through activation of Akt. Finally, molecular docking assay indicated the steady hydrogen bond was formed between Pae and Akt2. Experiments above suggested that Pae ameliorated glucose and lipid metabolism disorders and the underlying mechanism was closely related to the activation of Akt.

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Association of lipid profile test values, type-2 diabetes mellitus, and periodontitis

Cited by 11 publications

References 25 publications

<p>TLR4 Polymorphisms (896A>G and 1196C>T) Affect the Predisposition to Diabetic Nephropathy in Type 2 Diabetes Mellitus</p>

<p>TLR4 Polymorphisms (896A>G and 1196C>T) Affect the Predisposition to Diabetic Nephropathy in Type 2 Diabetes Mellitus</p>

Polydatin ameliorates lipid and glucose metabolism in type 2 diabetes mellitus by downregulating proprotein convertase subtilisin/kexin type 9 (PCSK9)

Paeonol Ameliorates Glucose and Lipid Metabolism in Experimental Diabetes by Activating Akt

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