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October 18, 2022DiabetesOpen Access

Endothelial-Specific Expression of CIDEC Improves High-Fat Diet–Induced Vascular and Metabolic Dysfunction

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Key result

Endothelial-specific expression of human CIDEC in mice protected against high-fat diet-induced glucose intolerance, insulin resistance, and dyslipidemia by modulating VEGF signaling.

Why the study?

Endothelial CIDEC was recently found to regulate vascular function, but its physiological effects and molecular actions in controlling vascular phenotype and whole-body glucose homeostasis remained to be characterized.

Does endothelial-specific expression of CIDEC improve high-fat diet-induced vascular and metabolic dysfunction in mice?

Population

Humanized mouse model expressing endothelial-specific human CIDEC (E-CIDECtg)

Design

Preclinical animal model study

Authors

BBBijinu BalakrishnanOhio UniversityAGAbhishek GuptaCentral Drug Research InstituteRBRabia BasriOhio University

Discussion

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Implication

Hypothesis-generating for endothelial CIDEC as a cardiometabolic target; requires human validation before clinical consideration.

Structured PICO

Does endothelial-specific expression of CIDEC improve high-fat diet-induced vascular and metabolic dysfunction in mice?

P
Population
Mouse model on a high-fat diet
I
Intervention
Endothelial-specific expression of human CIDEC (E-CIDECtg)
C
Comparator
Control mice on a high-fat diet
O
Outcome
Vascular phenotype and whole-body glucose homeostasissurrogate

Endothelial CIDEC protects against obesity-induced metabolic and vascular dysfunction by modulating VEGF signaling, highlighting it as a potential therapeutic target for cardiometabolic disease.

Cite This Study

Balakrishnan et al. (2022) studied High-fat diet-induced vascular and metabolic dysfunction. Endothelial-specific human CIDEC expression was evaluated on Glucose intolerance, insulin resistance, dyslipidemia, and vascular function. Endothelial-specific expression of human CIDEC in mice protected against high-fat diet-induced glucose intolerance, insulin resistance, and dyslipidemia by modulating VEGF signaling.

synapsesocial.com/papers/6a1d7bb2cc9f7df1b705826bhttps://doi.org/10.2337/db22-0294
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