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HORMONAL CHANGES AND INSULIN RESISTANCE: MECHANISMS OF
GESTATIONAL DIABETES DEVELOPMENT
Jo’rayeva Gulhayo Jalol qizi
Asian International University.
https://doi.org/10.5281/zenodo.15737607
Abstract
. Gestational diabetes mellitus (GDM) is a common pregnancy-related metabolic
disorder characterized by glucose intolerance first recognized during pregnancy. Its
pathophysiology is primarily rooted in insulin resistance, which is largely driven by hormonal
changes unique to pregnancy. Elevated levels of placental hormones such as human placental
lactogen (hPL), cortisol, estrogen, and progesterone interfere with insulin signaling, thereby
reducing maternal insulin sensitivity. In most women, pancreatic β
-cells compensate by
increasing insulin secretion; however, in genetically or metabolically predisposed individuals,
this compensation is insufficient, resulting in hyperglycemia and GDM. Understanding the
complex endocrine mechanisms underlying GDM is crucial for early diagnosis, management,
and prevention of maternal and neonatal complications. This article reviews the hormonal basis
of insulin resistance during pregnancy and outlines the key stages of gestational diabetes
development.
Keywords:
gestational diabetes, insulin resistance, pregnancy hormones, human
placental lactogen, cortisol, β
-cell dysfunction, hyperglycemia, early diagnosis, maternal health,
fetal complications
Introduction
Gestational diabetes mellitus (GDM) is a type of glucose intolerance that is first
recognized during pregnancy. While often temporary, it carries significant implications for both
maternal and fetal health. The global incidence of GDM is rising, largely due to changes in
lifestyle, increased maternal age, and a higher prevalence of obesity. The development of GDM
is primarily linked to
insulin resistance
, which is induced by the hormonal shifts that occur
naturally during pregnancy. This article explores the endocrine mechanisms behind GDM,
focusing on how hormonal changes contribute to insulin resistance.
Hormonal Changes in Pregnancy: A Physiological Adaptation
•
Pregnancy triggers a complex cascade of hormonal changes designed to support fetal
development and maintain gestation. These hormones also impact the mother's metabolism by
reducing her sensitivity to insulin
—
a physiological adaptation that ensures more glucose is
available to the fetus.
Key Hormones That Increase During Pregnancy:
•
Human placental lactogen (hPL)
•
Cortisol
•
Estrogen and progesterone
•
Prolactin
•
Leptin and resistin (from adipose tissue)
These hormones act collectively to
reduce insulin sensitivity
in peripheral tissues,
especially muscle and adipose tissue. While this is a normal response, in some women, it
becomes excessive and leads to GDM.
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Mechanisms of Insulin Resistance in Pregnancy
Insulin is a hormone secreted by pancreatic
β
-cells that facilitates glucose uptake into
cells, thereby reducing blood glucose levels. During pregnancy, maternal tissues naturally
become less responsive to insulin, prompting the pancreas to increase insulin production to
maintain euglycemia.
However, when this
compensatory response is inadequate
, glucose levels rise, resulting
in gestational diabetes. This imbalance is particularly likely in women with:
•
A family history of type 2 diabetes
•
Obesity or high BMI
•
Polycystic ovary syndrome (PCOS)
•
A history of GDM in previous pregnancies
Role of Specific Hormones in Insulin Resistance
1.
Human Placental Lactogen (hPL)
Secreted by the placenta, hPL increases progressively throughout pregnancy. It
antagonizes insulin
, reducing its effectiveness and promoting lipolysis and glucose availability
for the fetus. Elevated hPL is a key contributor to insulin resistance.
2.
Cortisol
A glucocorticoid hormone from the adrenal glands, cortisol levels rise significantly
during pregnancy. Cortisol promotes
gluconeogenesis
and
inhibits insulin action
, contributing
to hyperglycemia.
3.
Progesterone and Estrogen
These sex hormones increase insulin resistance by modifying insulin receptor signaling.
Progesterone also affects pancreatic
β
-cell function, but may not fully compensate for rising
glucose demands.
4.
Leptin and Resistin
These adipokines, produced by fat tissue, interfere with insulin signaling pathways.
Leptin resistance, common in obesity, may further exacerbate metabolic imbalance during
pregnancy.
Stages of Gestational Diabetes Development
1.
Hormonal rise during pregnancy
→ decreased insulin sensitivity
2.
Compensatory hyperinsulinemia
by the pancreas
3.
β
-cell dysfunction or exhaustion
in predisposed women
4.
Resultant hyperglycemia
(high blood glucose levels)
5.
Diagnosis of GDM
, usually between 24
–
28 weeks of gestation via Oral Glucose
Tolerance Test (OGTT)
Complications of Gestational Diabetes
•
If not properly managed, GDM can result in several complications:
For the mother:
•
Hypertension and preeclampsia
•
Increased risk of cesarean delivery
•
Future development of type 2 diabetes
For the fetus/newborn:
•
Macrosomia (excessive birth weight)
•
Neonatal hypoglycemia
•
Respiratory distress
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ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 6
•
Long-term risk of obesity and metabolic disorders
Conclusion
Gestational diabetes is a multifactorial condition rooted in the
hormonal and metabolic
changes
of pregnancy. While insulin resistance is a normal part of pregnancy, some women fail
to compensate adequately, leading to GDM. Understanding the endocrine mechanisms
—
especially the roles of placental and maternal hormones
—
is key to early detection, prevention,
and effective management of GDM. With proper screening and lifestyle interventions, the risks
associated with gestational diabetes can be significantly minimized, ensuring better outcomes for
both mother and child.
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