Study of Possible Relation between Fasting Plasma Glucagon, Gestational Diabetes and Development of Type 2 DM

Abstract

Background and Aims: Women who develop GDM (gestational diabetes mellitus) have a relative insulin secretion deficiency, the severity of which may be predictive for later development of diabetes. This study aimed to investigate the role of fasting plasma glucagon in the prediction of later development of diabetes in pregnant women with GDM. Materials and Methods: The study was conducted on 150 pregnant women with GDM after giving informed oral and written consents and being approved by the research ethical committee according to the declaration of Helsinki. The study was conducted in two phases, first phase during pregnancy and the second one was 6 months post-partum, as we measured fasting plasma glucagon before and after delivery together with fasting and 2 hour post-prandial plasma sugar. Results: Our findings suggested that glucagon levels significantly increased after delivery in the majority 14/25 (56%) of GDM women who developed type 2 DM within 6 months after delivery compared to 6/20 (30%) patients with impaired fasting plasma glucose (IFG) and only 22/105 (20%) non DM women, as the median glucagon levels were 80,76, 55, respectively. Also, there was a high statistical difference between fasting plasma glucagon post-delivery among diabetic and non-diabetic women (p ≤ 0.001). These results indicated the useful role of assessing fasting plasma glucagon before and after delivery in patients with GDM to predict the possibility of type 2 DM. Conclusion: There is a relatively high glucagon level in GDM patients, which is a significant pathogenic factor in the incidence of subsequent diabetes in women with a history of GDM. This could be important in the design of follow-up programs for women with previous GDM.

Impairments of insulin and glucagon sensitivity in Chinese women with gestational diabetes mellitus

“…A handful of studies have suggested that hyperglucagonaemia may precede insulin resistance to disrupt glucose tolerance in GDM. 5,[30][31][32] Several limitations should be noted in our study. First, the sample size may be considered relatively small, but the primary outcomes of our study were clear-cut.…”

“…Augmented glucagon levels would be counterproductive in terms of controlling blood glucose in GDM. A handful of studies have suggested that hyperglucagonaemia may precede insulin resistance to disrupt glucose tolerance in GDM 5,30–32 …”

Postprandial Lipemia Modulates Pancreatic Alpha-Cell Function in the Prediction of Type 2 Diabetes Development: The CORDIOPREV Study

“…Our results agree with previous works reporting that alpha-cell dysfunction, evaluated by higher levels of glucagon, precedes T2DM development. 8,9,48,49 Other studies have also described that patients with a higher postprandial level of the glucagon:insulin ratio presented a higher probability of developing T2DM. 10,50 These results suggest that the use of challenge tests such as the OGTT are more suitable than static measurements in assessing the individual phenotypic flexibility and the potential risk of developing the metabolic disorder.…”

Glucagon, cyclic AMP, and hepatic glucose mobilization: A half‐century of uncertainty

“…One value in B (PV) was obtained by ELISA instead of RIA (Hussein et al, 1986). The data were compiled from the following references: A (Species)–Humans (H): Bolli et al (1984), Borghi et al (1984), Brodows (1985), Evans et al (2004), Fujita et al (1975), Gosmanov et al (2005), Hamaguchi et al (1991), Hansen et al (1982), Heise et al (2004), (2004), Henkel et al (2005), Jaspan et al (1984), Kalkhoff et al (1973), Livingston et al (1985), Okba et al (2020), Petersen and Sullivan (2001), Porcellati et al (2003), Raju and Cryer (2005), Sherwin et al (2005), Tasaka et al (1980), Verillo et al (1988); Dogs (D): Cersosimo et al(1998), Coker, Koyama, Brooks, et al (1999), Kraft et al (2017), Ishida et al (1983), Moore et al (2014), Sherck et al (2001), Sindelar et al (1998), and Vaitkus et al (1984); Rats (R): Balks and Jungermann (1984), Charbonneau et al (2005), Langhans et al (1984), Latour et al (1999), Mayor and Calle, (1988), Omer et al (2004), Powell et al (1993), Ruiter et al (2003), Unger (1985), Widmaier et al (1991) and Winzell et al (2007), Mice (M): Green et al (2016), Karlsson et al (2002), Marty et al (2005), Parker et al (2002), Perry et al (2020), Winzell et al (2007) and Zhang et al (2018) B (Vascular Bed) ‐ Hepatic Portal (HP): See legend, Figure 1, Peripheral Venous (PV): Balks and Jungermann (1984), Bolli et al (1984), Cersosimo et al (1998), Charbonneau et al (2005), Coker, Koyama, Brooks, et al (1999…”