open access

Ahead of print
Original paper
Published online: 2021-04-08
Submitted: 2020-11-26
Accepted: 2021-02-15
Get Citation

Insulin resistance in metabolic syndrome depending on the occurrence of its components.

Marcin Arkadiusz Gierach, Roman Junik
DOI: 10.5603/EP.a2021.0037

open access

Ahead of print
Original Paper
Published online: 2021-04-08
Submitted: 2020-11-26
Accepted: 2021-02-15

Abstract

Metabolic syndrome (MetS) is described as a cluster of several commonly occurring disorders including abdominal obesity, hypertension (HT) (≥130/85 mmHg), carbohydrates disorders: impaired fasting glucose or type 2 diabetes mellitus and lipids disorders such as hypertriglyceridemia (TG) and low level of high-density-lipoprotein cholesterol (HDL-C). Insulin resistance (IR) is defined as a glucose homoeostasis disorder involving a decreased sensitivity of muscles, adipose tissue, liver and other body tissues to insulin, despite its normal or increased concentration in blood. The study group included 424 subjects with MetS (260 females, 164 males). All patients were recruited from the Internal Ward of the District Hospital in Wąbrzeźno, Poland and Department of Endocrinology and Diabetology Collegium Medicum in Bydgoszcz, Poland. The diagnosis of the MetS was made on the basis of the International Diabetes Federation (IDF) criteria. MetS diagnosis was established when three or more criteria were met. The study group was divided into 6 subgroups according to the constellation of 3 particular components of MetS. All patients of the study group were diagnosed with obesity, 73,5% with high pre-meal blood glucose levels, 66.9% with HT, 48.3% with lower level of HDL-C and 38.2% with TG. Insulin resistance of different degree was diagnosed in all patients of the study group. The occurrence of insulin resistance in patients with metabolic syndrome is obvious. However, despite they are high or very high cardiovascular risk patients, they are not a homogeneous group. Such patients differ from each other depending on the presence and constellation of particular disorders that make up the diagnosis of the metabolic syndrome. Patients with MetS are heterogeneous group differing in degree of insulin resistance and the risk of cardiovascular diseases. The results of our study show that the highest insulin resistance is observed in patients with central obesity accompanied by type 2 diabetes and hypertriglyceridemia.

Abstract

Metabolic syndrome (MetS) is described as a cluster of several commonly occurring disorders including abdominal obesity, hypertension (HT) (≥130/85 mmHg), carbohydrates disorders: impaired fasting glucose or type 2 diabetes mellitus and lipids disorders such as hypertriglyceridemia (TG) and low level of high-density-lipoprotein cholesterol (HDL-C). Insulin resistance (IR) is defined as a glucose homoeostasis disorder involving a decreased sensitivity of muscles, adipose tissue, liver and other body tissues to insulin, despite its normal or increased concentration in blood. The study group included 424 subjects with MetS (260 females, 164 males). All patients were recruited from the Internal Ward of the District Hospital in Wąbrzeźno, Poland and Department of Endocrinology and Diabetology Collegium Medicum in Bydgoszcz, Poland. The diagnosis of the MetS was made on the basis of the International Diabetes Federation (IDF) criteria. MetS diagnosis was established when three or more criteria were met. The study group was divided into 6 subgroups according to the constellation of 3 particular components of MetS. All patients of the study group were diagnosed with obesity, 73,5% with high pre-meal blood glucose levels, 66.9% with HT, 48.3% with lower level of HDL-C and 38.2% with TG. Insulin resistance of different degree was diagnosed in all patients of the study group. The occurrence of insulin resistance in patients with metabolic syndrome is obvious. However, despite they are high or very high cardiovascular risk patients, they are not a homogeneous group. Such patients differ from each other depending on the presence and constellation of particular disorders that make up the diagnosis of the metabolic syndrome. Patients with MetS are heterogeneous group differing in degree of insulin resistance and the risk of cardiovascular diseases. The results of our study show that the highest insulin resistance is observed in patients with central obesity accompanied by type 2 diabetes and hypertriglyceridemia.

Get Citation

Keywords

metabolic syndrome, insulin resistance, diabetes mellitus, obesity

About this article
Title

Insulin resistance in metabolic syndrome depending on the occurrence of its components.

Journal

Endokrynologia Polska

Issue

Ahead of print

Article type

Original paper

Published online

2021-04-08

DOI

10.5603/EP.a2021.0037

Keywords

metabolic syndrome
insulin resistance
diabetes mellitus
obesity

Authors

Marcin Arkadiusz Gierach
Roman Junik

References (15)
  1. Rochlani Y, Pothineni NV, Kovelamudi S, et al. Metabolic syndrome: pathophysiology, management, and modulation by natural compounds. Ther Adv Cardiovasc Dis. 2017; 11(8): 215–225.
  2. Gierach M, Gierach J, Junik R, et al. Hashimoto's thyroiditis and carbohydrate metabolism disorders in patients hospitalised in the Department of Endocrinology and Diabetology of Ludwik Rydygier Collegium Medicum in Bydgoszcz between 2001 and 2010. Endokrynol Pol. 2012; 63(1): 14–17.
  3. Bonora E, Kiechl S, Willeit J, et al. Bruneck study, Bruneck Study, Bruneck study. Prevalence of insulin resistance in metabolic disorders: the Bruneck Study. Diabetes. 1998; 47(10): 1643–1649.
  4. Gast KB, Tjeerdema N, Stijnen T, et al. Insulin resistance and risk of incident cardiovascular events in adults without diabetes: meta-analysis. PLoS One. 2012; 7(12): e52036.
  5. Juárez-López C, Klünder-Klünder M, Medina-Bravo P, et al. Insulin resistance and its association with the components of the metabolic syndrome among obese children and adolescents. BMC Public Health. 2010; 10: 318.
  6. Abbasi F, Kohli P, Reaven GM, et al. Hypertriglyceridemia: A simple approach to identify insulin resistance and enhanced cardio-metabolic risk in patients with prediabetes. Diabetes Res Clin Pract. 2016; 120: 156–161.
  7. Ginsberg HN. Insulin resistance and cardiovascular disease. J Clin Invest. 2000; 106(4): 453–458.
  8. Ormazabal V, Nair S, Elfeky O, et al. Association between insulin resistance and the development of cardiovascular disease. Cardiovasc Diabetol. 2018; 17(1): 122.
  9. Natali A, Santoro D, Palombo C, et al. Impaired insulin action on skeletal muscle metabolism in essential hypertension. Hypertension. 1991; 17(2): 170–178.
  10. Zhou MS, Wang A, Yu H. Link between insulin resistance and hypertension: What is the evidence from evolutionary biology? Diabetol Metab Syndr. 2014; 6(1): 12.
  11. Roden M, Price TB, Perseghin G, et al. Mechanism of free fatty acid-induced insulin resistance in humans. J Clin Invest. 1996; 97(12): 2859–2865.
  12. Rocchini AP, Yang JQ, Gokee A, et al. The relationship of sodium sensitivity to insulin resistance. Am J Med Sci. 1994; 307 Suppl 1(5): S75–S80.
  13. DeFronzo RA, Cooke CR, Andres R, et al. The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. J Clin Invest. 1975; 55(4): 845–855.
  14. Schoonjans K, Staels B, Auwerx J. The peroxisome proliferator activated receptors (PPARs) and their effects on lipid metabolism and adipocyte differentiation. Biochim Biophys Acta (BBA) — Lipids and Lipid Metabolism. 1996; 1302(2): 93–109.
  15. Paneni F, Costantino S, Cosentino F. Role of oxidative stress in endothelial insulin resistance. World J Diabetes. 2015; 6(2): 326–332.

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

Via MedicaWydawcą serwisu jest  "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl