Vol 72, No 3 (2021)
Original paper
Published online: 2021-04-08

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

Marcin Gierach12, Roman Junik1
Pubmed: 34010436
Endokrynol Pol 2021;72(3):243-248.

Abstract

Introduction: Metabolic syndrome (MetS) is described as a cluster of several commonly occurring disorders including abdominal obesity, hypertension (HT) (≥ 130/85 mm Hg), carbohydrate disorders: impaired fasting glucose or type 2 diabetes mellitus and lipids disorders such as hypertriglyceridaemia (TG), and low levels 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.

Material and methods: The study group included 424 subjects with MetS (260 females, 164 males). All patients were recruited for 24 months from the Internal Ward of the District Hospital in Wąbrzeźno, Poland and the Department of Endocrinology and Diabetology Collegium Medicum in Bydgoszcz, Poland. The diagnosis of the MetS was made on the basis of International Diabetes Federation (IDF) criteria. MetS diagnosis was established when three or more criteria were met. To evaluate and measure IR, a hyperinsulinaemic-euglycaemic clamp was performed in each patient. IR was also determined through HOMA-IR.

Results: All patients of the study group were diagnosed with obesity, 73.5% with high fasting glucose levels, 66.9% with HT, 48.3% with lower level of HDL-C, and 38.2% with TG. It did not have an influence on the IR results. The study group was divided into 6 subgroups according to the constellation of 3 particular components of MetS (O + DM2T + ↑TG; O + HT + DM2T; O + DM2T + ↓HDL-C; O + HT + IFG; O + HT + ↑TG and O + HT + ↓HDL-C). IR of different degree was diagnosed in all patients of the study group. The results of our study showed that the highest IR was observed in patients with central obesity accompanied by DM2T and ↑TG. Also in subgroups with DM2T and HT or DM2T and ↓HDL-C, a high index of IR was noticed.

Conclusions: The occurrence of IR in patients with MetS is obvious. However, despite the fact that 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 MetS. Patients with MetS are a heterogeneous group differing in degree of IR and the risk of CVD. 

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References

  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.