Insulin Resistance and the Metabolic Syndrome Severity
– a Mathematical Model
Elizabeth KERTOWIDJOJO1, Dumitru
Andrei IACOBAŞ2,3,4
1 Assistant
Professor, MD, PhD, Department
of Pathology, University of Chicago, Chicago,
IL 60637, U.S.A.
2Research Professor, PhD. Director Personalized
Genomics Laboratory, Center for Computational Systems
Biology, Prairie View A&M University, Prairie View, TX 77407, U.S.A.
(daiacobas@pvamu.edu)
3 Professor Emeritus, “Ovidius” University, Constanta
4 Honorary Member, Academy of Romanian Scientists
Abstract.
Excessive fructose consumption was shown to have deleterious effects on the
cardiovascular system, particularly as the metabolic syndrome. However, the
degree by which alteration of each pathophysiological factor contributes to the
morbidity associated with fructose consumption is not yet clear. We have
developed a mathematical model to integrate and uniformly quantify
pathophysiological features of the metabolic syndrome on a high fructose-fed
dog model. A novel comprehensive measure for the syndrome severity (the “patholog”) and a more intuitive measure of the insulin
resistance are introduced. Alteration of hemodynamics, echocardiography and
blood chemistry were determined in adult male mongrel dogs fed with 60%
isocaloric fructose or normal chow for 7 weeks. The diverse experimental data
were transformed into comparable scores and a pre-Hilbert space of states
constructed. In such a space one can quantify the severity of any combination
of pathophysiological and genomic features and determine the global recovery resulting
from a treatment. The model indicates increase of insulin resistance (new index
proposed), systolic blood pressure, low-to-high density lipids ratio and
angiotensin II as the major contributors to the excessive fructose morbidity.
Our model provides the simplest, yet the most intuitive and comprehensive way
to integrate data of a wide diversity in visualizing and quantifying a
cardiovascular disease.
Key
words: Fructose consumption, Cholesterol, Insulin resistance,
Angiotensin II, Dog model
DOI https://doi.org/10.56082/annalsarscibio.2022.1.91
