Hyperinsulinemia promotes endothelial inflammation via increased expression and release of Angiopoietin-2

Chandel, Shivam; Sathis, Anuradha; Dhar, Monalisa; Giri, Hemant; Nathan, Abel Arul; Samawar, Sai Kiran Reddy; Gupta, Akshari; Gopal, Jayashree; Ranjani, Harish; Mohan, Viswanathan; Dixit, Madhulika

doi:10.1016/j.atherosclerosis.2020.06.016

Cited by 21 publications

(20 citation statements)

References 64 publications

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“…Thus, insulin maintains metabolism and energy stores in our body; however, too much of a good thing may be harmful. This is the case of hyperinsulinemia 58–63 . Hyperinsulinemia is an independent risk factor for hypertension, atherosclerosis, dyslipidemia, endothelial dysfunction, CVDs, obesity, and T2DM 58–63 .…”

Section: Insulin Resistance Disordersmentioning

confidence: 99%

“…This is the case of hyperinsulinemia 58–63 . Hyperinsulinemia is an independent risk factor for hypertension, atherosclerosis, dyslipidemia, endothelial dysfunction, CVDs, obesity, and T2DM 58–63 . Figure 2B depicts the relationship between hyperinsulinemia, IR, metabolic syndrome, obesity, dyslipidemia, atherosclerosis, T2DM, and CVDs.…”

Section: Insulin Resistance Disordersmentioning

confidence: 99%

“…T2DM patients suffer many macrovascular and microvascular complications wherein CVDs are the most common 99,55 . In reality, the sustained state of the (IR ↔ hyperinsulinemia) vicious cycle preceding the development of hyperglycemia and the diagnosis of T2DM is one of the root causes of many T2DM complications such as atherogenic dyslipidemia, diabetic cardiomyopathy, CVDs, infectious diseases, and cancer 99,52,55,100,8,95,58–63 (Figure 2B).…”

Section: Insulin Resistance Disordersmentioning

confidence: 99%

“…This atherogenic dyslipidemia is highly derived by IR and hyperinsulinemia 113–116 . IR is associated with platelets and endothelial dysfunctions which increase the risk of developing CVDs in IR disorder patients 77,78,62,59 . Moreover, hyperinsulinemia increases the risk of developing CVDs 117 .…”

Section: Cardiovascular Diseases Metabotypesmentioning

confidence: 99%

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The metabolic signatures of cardiometabolic diseases: Does the shared metabotype offer new therapeutic targets?

Amin

2021

Lifestyle Medicine

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Cardiometabolic diseases (CMDs) are the most common, noncommunicable diseases that claim many lives every year. CMDs have great impact on public health, often driving the attention of healthcare resources to prevent and treat them. CMDs include cardiovascular diseases, type 2 diabetes mellitus, metabolic syndrome, and obesity. Deep understanding of the root causes and pathogenic factors of CMDs would help in their effective prevention and treatment. Metabolomic profiling of biosamples usually sheds light on the metabolic biomarkers and the involved pathways. Metabolomic analysis to identify CMDs metabotypes revealed that they share similar metabolic signatures and metabolic pathways. These metabolic pathways may indicate the presence of insulin resistance, mitochondrial dysfunction, low‐grade inflammation, and dysbiotic gut microbiota. This study is aimed to review the literature on the common metabolic biomarkers of CMDs as well as the shared pathways that can be targeted by dietary interventions and pharmacologic treatment.

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Section: Insulin Resistance Disordersmentioning

confidence: 99%

Section: Insulin Resistance Disordersmentioning

confidence: 99%

Section: Insulin Resistance Disordersmentioning

confidence: 99%

Section: Cardiovascular Diseases Metabotypesmentioning

confidence: 99%

See 2 more Smart Citations

The metabolic signatures of cardiometabolic diseases: Does the shared metabotype offer new therapeutic targets?

Amin

2021

Lifestyle Medicine

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“…The emergence of chronic metabolic disorders, such as type 2 diabetes mellitus (T2DM), was shown to increase the risk of atherosclerotic plaques development [5]. The increase of insulin levels (hyperinsulinemia) intensi es the formation of atherosclerotic plaques in addition to disturbances in lipid metabolism seen under diabetic conditions [6,7]. Therefore, one could hypothesize that atherosclerotic plaques are developed in response to different stimuli.…”

Section: Introductionmentioning

confidence: 99%

Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

Abriz

Rahbarghazi‬

Nourazarian

et al. 2020

Preprint

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Background: Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods: Human umbilical vein endothelial cells were treated with 1mM palmitic acid, 50μM insulin, 50μM docosahexaenoic acid, and their combination for 48 hours. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results: Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin blunted palmitic acid detrimental effects on HUVECs indicated by an increased survival rate (p<0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p<0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p<0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p<0.05). PCR array analysis revealed the modulatory effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p<0.05). Conclusion: DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro

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Endothelial dysfunction: molecular mechanisms and clinical implications

Wang,

2024

MedComm

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Cardiovascular disease (CVD) and its complications are a leading cause of death worldwide. Endothelial dysfunction plays a crucial role in the initiation and progression of CVD, serving as a pivotal factor in the pathogenesis of cardiovascular, metabolic, and other related diseases. The regulation of endothelial dysfunction is influenced by various risk factors and intricate signaling pathways, which vary depending on the specific disease context. Despite numerous research efforts aimed at elucidating the mechanisms underlying endothelial dysfunction, the precise molecular pathways involved remain incompletely understood. This review elucidates recent research findings on the pathophysiological mechanisms involved in endothelial dysfunction, including nitric oxide availability, oxidative stress, and inflammation‐mediated pathways. We also discuss the impact of endothelial dysfunction on various pathological conditions, including atherosclerosis, heart failure, diabetes, hypertension, chronic kidney disease, and neurodegenerative diseases. Furthermore, we summarize the traditional and novel potential biomarkers of endothelial dysfunction as well as pharmacological and nonpharmacological therapeutic strategies for endothelial protection and treatment for CVD and related complications. Consequently, this review is to improve understanding of emerging biomarkers and therapeutic approaches aimed at reducing the risk of developing CVD and associated complications, as well as mitigating endothelial dysfunction.

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Hyperinsulinemia promotes endothelial inflammation via increased expression and release of Angiopoietin-2

Cited by 21 publications

References 64 publications

The metabolic signatures of cardiometabolic diseases: Does the shared metabotype offer new therapeutic targets?

The metabolic signatures of cardiometabolic diseases: Does the shared metabotype offer new therapeutic targets?

Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

Endothelial dysfunction: molecular mechanisms and clinical implications

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