Loading...
Please wait, while we are loading the content...
Insulin Resistance in the Third Trimester of Pregnancy Suffering from Gestational Diabetes Mellitus or Impaired Glucose Tolerance
| Content Provider | Semantic Scholar |
|---|---|
| Author | Shalayel, Mohammed K. N. Shubair And Mohammed H. F. Al-Noaemi, Mohammed Chyad |
| Copyright Year | 2012 |
| Abstract | Pregnancy results in a state of insulin resistance (Dahlgren, 2006) that appears to include a decrease in maximum insulin sensitivity or responsivity (Baban et al., 2010). This insulin resistance abates in the postpartum period (Kuhl, 1991). Insulin resistance is defined as the decrease of the biological action of insulin (Catalano, 2010; Robert, 1995), and it mainly presents as hyperinsulinemia (Baban et al., 2010; Robert, 1995) or decreased ability of insulin to regulate glucose utilization (Kim et al., 1996). The resistance to insulin can be characterized as pre-receptor (insulin antibodies), receptor (decreased number of receptors on the cell surface), or post-receptor (defects in the intracellular insulin signaling pathway). In pregnancy, the decreased insulin sensitivity is best characterized as a post-receptor defect resulting in the decreased ability of insulin to bring about glucose transporter (GLUT4) mobilization from the interior of the cell to the cell surface (Catalano, 2010). Most pregnant women are able to counteract the insulin resistance state by increasing their insulin secretion. However, when the capacity of insulin secretion is not sufficiently large to meet the insulin resistance, glucose intolerance develops and the women develop gestational diabetes (Kuhl et al., 1985). Gestational diabetes mellitus (GDM) is defined as a carbohydrate intolerance of varying severity with onset or first recognition during the present pregnancy (Kaaja & Rönnemaa, 2008; Damm et al., 1994; Summary and recommendation of the second international workshop conference of gestational diabetes, 1985; Shalayel et al., 2010). GDM has onset or discovery of glucose intolerance during pregnancy (Reece et al., 2009), usually in the second or third trimester (Shalayel et al., 2007). GDM carries long-term implications for the subsequent development of type 2 diabetes in the mother and increased risk for obesity and glucose intolerance in the offspring (Barbour et al., 2007). The world health organization defines diabetes in pregnancy as a fasting glucose ≥ 7.9 mmol/L or a value >11 mmol/L 2hour after a 75g glucose load (Shalayel et al., 2010; Campbell & Lees, 2000). |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://cdn.intechweb.org/pdfs/23180.pdf |
| Alternate Webpage(s) | http://cdn.intechopen.com/pdfs-wm/23180.pdf |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Alkhurma virus Carbohydrates Cut, copy, and paste Damm algorithm Diabetes Mellitus Diabetes Mellitus, Non-Insulin-Dependent Exercise Fax Gene regulatory network Gestational Diabetes Glucose Transporter Hyperglycemia Hyperinsulinism Impaired glucose tolerance Incidence matrix Insulin Antibodies Insulin Resistance Insulin/Insulin Receptor Signaling Pathway International Standard Book Number NSA product types Onset (audio) Page (document) Pregnancy in Diabetics REV Robert Scientific Publication Signal Transduction Software bug The Offspring WDFY2 wt Allele Word lists by frequency insulin secretion insulin, isophane millimole |
| Content Type | Text |
| Resource Type | Article |
