Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021 Jun 16;21(1):124.
doi: 10.1186/s12902-021-00788-5.

Impact of triglycerides and waist circumference on insulin resistance and β-cell function in non-diabetic first-degree relatives of type 2 diabetes

Affiliations

Impact of triglycerides and waist circumference on insulin resistance and β-cell function in non-diabetic first-degree relatives of type 2 diabetes

Fahd Ahmed et al. BMC Endocr Disord. .

Abstract

Background: Although there is abundant evidence indicating the relative contribution of insulin resistance (HOMA-IR) and β-cell dysfunction (HOMA-β) among first-degree relatives (FDRs) of Type 2 DM patients, few studies reported the association between HOMA-IR and HOMA-β with metabolic syndrome. Our objective was to evaluate the impact of metabolic syndrome factors on HOMA-IR, HOMA-β and glycoproteins in non-diabetic FDRs.

Methods: In this study, 103 Yemeni male subjects aged 25-42 years, with BMI < 25 kg/m2 were examined, 39 of whom were normal subjects with no family history of diabetes served as control and 64 subjects were non-diabetic FDRs of Type 2 DM patients.

Results: Both glycoproteins, glycated haemoglobin (HbA1c) and fructosamine as well as insulin, HOMA-IR and HOMA-β were significantly (p = 4.9 × 10-9; 6.0 × 10-8; 6.6 × 10-12; 1.3 × 10-7; 5.5 × 10-12, respectively) higher in non-diabetic FDRs as compared to control group. Fasting plasma glucose, though within normal range, were significantly (p = 0.026) higher in non-diabetic FDRs. Linear regression analysis showed that both TG and WC are the main metabolic syndrome factors that significantly increased HOMA-IR (B = 0.334, p = 1.97 × 10-6; B = 0.024, p = 1.05 × 10-5), HOMA-β (B = 16.8, p = 6.8 × 10-5; B = 0.95, p = 0.004), insulin (B = 16.5, p = 1.2 × 10-6; B = 1.19, p = 8.3 × 10-6) and HbA1c (B = 0.001, p = 0.034; B = 0.007, p = 0.037).

Conclusion: Triglyceride and WC are the important metabolic syndrome factors associated with insulin resistance, basal β-cell function and insulin levels in non-diabetic FDR men of Type 2 DM patients. Moreover, FDRs showed insulin resistance with compensatory β-cell function (hyperinsulinaemia) suggesting that insulin resistance precede the development of pancreatic β-cell dysfunction in individuals at risk of Type 2 DM.

Keywords: First-degree relatives of Type 2 DM; Fructosamine; HbA1c; Insulin resistance; Metabolic syndrome; β-cell function.

PubMed Disclaimer

Conflict of interest statement

The authors have no conflict of interest to declare.

Similar articles

Cited by

References

    1. International Diabetes Federation . IDF diabetes atlas. 9. Brussels, Belgium: International Diabetes Federation; 2019. - PubMed
    1. Kahn SE, Cooper ME, Del Prato S. Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future. Lancet. 2014;383(9922):1068–1083. doi: 10.1016/S0140-6736(13)62154-6. - DOI - PMC - PubMed
    1. Norris SL, Kansagara D, Bougatsos C, Nygren P, Fu R. Screening for type 2 diabetes mellitus: update of 2003 systematic evidence review for the U.S. Preventive Services Task Force. AHRQ Publication No. 08-05116-EF-1, pp. 1–47; 2008.
    1. Leahy JL. Pathogenesis of type 2 diabetes mellitus. Arch Med Res. 2005;36:197–209. doi: 10.1016/j.arcmed.2005.01.003. - DOI - PubMed
    1. Wagner R, Thorand B, Osterhoff MA, Muller G, Bohm A, Meisinger C, et al. Family history of diabetes is associated with higher risk for prediabetes: a multicentre analysis from the German Center for Diabetes Research. Diabetologia. 2013;56(10):2176–2180. doi: 10.1007/s00125-013-3002-1. - DOI - PubMed

MeSH terms