Pancreatic beta cell function and insulin resistance profiles in first-degree relatives of patients with prediabetes and type 2 diabetes

被引:1
作者
Herrerias-Garcia, Anaid [1 ]
Jacobo-Tovar, Emmanuel [1 ]
Hernandez-Robles, Claudia Mariana [1 ]
Guardado-Mendoza, Rodolfo [1 ]
机构
[1] Univ Guanajuato, Dept Med & Nutr, Metab Res Lab, Blvd Milenio 1001, Leon 37670, Guanajuato, Mexico
关键词
Prediabetes; Type; 2; diabetes; Insulin sensitivity; Pancreatic beta cell dysfunction; Genetic predisposition; IMPAIRED FASTING GLUCOSE; RISK-FACTORS; PATHOPHYSIOLOGY; OBESITY; HERITABILITY; DYSFUNCTION; PREVENTION; PREDICTION; MEMBERS; GENOME;
D O I
10.1007/s00592-024-02352-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims To evaluate insulin secretion and insulin resistance profiles in individuals with family history of prediabetes and type 2 diabetes. Methods This was a cross-sectional study to evaluate clinical and metabolic profiles between individuals with type 2 diabetes, prediabetes and their relatives. There were 911 subjects divided into five groups: (i) normoglycemic (NG), (ii) type 2 diabetes, (iii) prediabetes, (iv) first-degree relatives of patients with type 2 diabetes (famT2D), and (v) first-degree relatives of patients with prediabetes (famPD); anthropometrical, biochemical and nutritional evaluation, as well as insulin resistance and pancreatic beta cell function measurement was performed by oral glucose tolerance to compare between groups. Results The most prevalent type 2 diabetes risk factors were dyslipidemia (81%), family history of type 2 diabetes (76%), central obesity (73%), male sex (63%), and sedentary lifestyle (60%), and most of them were progressively associated to prediabetes and type 2 diabetes groups. Insulin sensitivity was lower in famT2D groups in comparison to NG group (p < 0.0001). FamPD and famT2D had a 10% lower pancreatic beta cell function (DI) than the NG group (NG group 2.78 +/- 1.0, famPD 2.5 +/- 0.85, famT2D 2.4 +/- 0.75, p<0.001). Conclusions FamPD and famT2D patients had lower pancreatic beta cell function than NG patients, highlighting that defects in insulin secretion and insulin sensitivity appear long time before the development of hyperglycemia in patients genetically predisposed.
引用
收藏
页码:253 / 261
页数:9
相关论文
共 46 条
  • [1] Abbafati C, 2020, LANCET, V396, P1204
  • [2] Pathophysiology of prediabetes
    Abdul-Ghani, Muhammad A.
    DeFronzo, Ralph A.
    [J]. CURRENT DIABETES REPORTS, 2009, 9 (03) : 193 - 199
  • [3] American Diabetes Association, 2019, Clin Diabetes, V37, P11, DOI [10.2337/cdl8-0105, DOI 10.2337/CD18-0105]
  • [4] Prediabetes diagnosis and treatment: A review
    Bansal, Nidhi
    [J]. WORLD JOURNAL OF DIABETES, 2015, 6 (02) : 296 - 303
  • [5] Prediabetes and Cardiovascular Disease Pathophysiology and Interventions for Prevention and Risk Reduction
    Brannick, Ben
    Dagogo-Jack, Sam
    [J]. ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA, 2018, 47 (01) : 33 - +
  • [6] Assessment of Pancreatic beta-Cell Function: Review of Methods and Clinical Applications
    Cersosimo, Eugenio
    Solis-Herrera, Carolina
    Trautmann, Michael E.
    Malloy, Jaret
    Triplitt, Curtis L.
    [J]. CURRENT DIABETES REVIEWS, 2014, 10 (01) : 2 - 42
  • [7] Pathogenesis of type 2 diabetes mellitus
    DeFronzo, RA
    [J]. MEDICAL CLINICS OF NORTH AMERICA, 2004, 88 (04) : 787 - +
  • [8] Type 2 diabetes mellitus
    DeFronzo, Ralph A.
    Ferrannini, Ele
    Groop, Leif
    Henry, Robert R.
    Herman, William H.
    Holst, Jens Juul
    Hu, Frank B.
    Kahn, C. Ronald
    Raz, Itamar
    Shulman, Gerald I.
    Simonson, Donald C.
    Testa, Marcia A.
    Weiss, Ram
    [J]. NATURE REVIEWS DISEASE PRIMERS, 2015, 1
  • [9] From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus
    DeFronzo, Ralph A.
    [J]. DIABETES, 2009, 58 (04) : 773 - 795
  • [10] Heritability of pancreatic β-cell function among nondiabetic members of Caucasian familial type 2 diabetic kindreds
    Elbein, SC
    Hasstedt, SJ
    Wegner, K
    Kahn, SE
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1999, 84 (04) : 1398 - 1403