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Review
. 2024 Apr;39(2):168-178.
doi: 10.1007/s12291-023-01157-w. Epub 2023 Oct 13.

Obesity: An Impact with Cardiovascular and Cerebrovascular Diseases

Savi Dutta  1 , A K Singhal  1   2 , Varsha Suryan  1   3 , Nimai Chand Chandra  1
Affiliations
Review

Obesity: An Impact with Cardiovascular and Cerebrovascular Diseases

Savi Dutta et al. Indian J Clin Biochem. 2024 Apr.

Abstract

The authors sought to correlate the complex sequel of obesity with various parameters known to develop metabolic syndrome viz. insulin resistance, dyslipidemia, hypertension etc., as these anomalies are linked to vascular atherosclerosis and outbreak of cardiovascular and cerebrovascular diseases. A comprehensive online survey using MEDLINE, Scopus, PubMed and Google Scholar was conducted for relevant journals from 1970 till present time (2023) with key search terms like: 'obesity', 'leptin', type-2 diabetes', 'atherosclerosis', 'cardiovascular and cerebrovascular diseases'. The findings of the reports were compared and correlated. The information was then collated for developing this review. Reports showed that in human obesity, hyper-leptinemia could induce hyperglycemia, which in turn templates hypercholesterolemia. Persisting hypercholesterolemia over a period of time may en-route atherosclerosis in blood vessels. Thus obesity has been considered as a template for originating hyperglycemia, hypercholesterolemia and outbreak of vascular atherogenesis or in other words, obesity in long run can trigger atherosclerosis and its related disorders e.g. heart attack and stroke. Literature survey shows that primarily, co-morbidities of human obesity start with leptin and insulin resistance and then multiplies with metabolic irregularities to an extreme that results in pathogenesis of heart attack and stroke. Atherosclerosis associated cardiovascular and cerebrovascular events are independent risks of obese subjects and particularly in the cases of persisting obesity.

Keywords: Atherosclerosis; Cardiovascular disease; Cerebrovascular disease; Leptin; Obesity; Type-2 diabetes.

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Conflict of interest statement

Conflict of interestThe authors declare that there is no conflict of interests.

Figures

Fig. 1
Fig. 1
Pathophysiology of obesity onset metabolic consequences
Fig. 2
Fig. 2
Common signalling pathway of insulin receptor (IR) and leptin receptor (OB-R). IRS: Insulin receptor substrate, PI3Kinase: Phosphoinositide3-kinase, Akt: Protein kinase B, STAT3: Signal transducers and activators of transcription, mTOR: Mammalian target of rapamycin
Fig. 3
Fig. 3
Insulin signalling for GLUT4 activation. IR: Insulin receptor, GLUT4: Glucose transporter4, PI3K: Phosphoinositide3-kinase, Akt: Protein kinase-B, GSV: GLUT4 storage vesicle, TXNIP: Thioredoxin interacting protein
Fig. 4
Fig. 4
Hyperglycemia and hypercholesterolemia induced atherosclerosis. IR: Insulin receptor, LDL: Low density lipoprotein, LDLR: LDL receptor, TG: Triacylglycerol
Fig. 5
Fig. 5
Atherosclerosis induced coronary artery disease and brain stroke
Fig. 6
Fig. 6
Metabolism of HDL and reverse cholesterol transport from tissue periphery. LDL: Low density lipoprotein, VLDL: Very low density lipoprotein, HDL: High density lipoprotein, C: Cholesterol, PL: Phospholipid, SR-A1: Scavenger receptor-class A1, SR-B1: Scavenger receptor-class B1, HL: Hepatic lipase, LOX-1: Receptor of oxidized LDL, OX-LDL: Oxidized LDL
See this image and copyright information in PMC

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