Table 3.

Physiologic and clinical effects of obesity on labor

Effect of obesity on labor physiology	Clinical observation	Possible physiologic mechanism
Disruption of endocrine signaling initiating labor onset	Delayed onset of parturition	Decreased CRH leading to inhibited functional progesterone withdrawal[55]
	Decreased cervical ripening	Elevated leptin disrupts collagen degradation and cervical cell apoptosis[61, 62]
	Decreased spontaneous rupture of membranes	Elevated leptin inhibits membrane apoptosis[61, 62]
Disruption of uterine contractility	Inadequate uterine contractions leading to increased risk for active phase cesarean	Elevated leptin, visfatin, and apelin inhibit spontaneous and oxytocin augmented uterine contractility in rats in vitro[43, 61, 62]
		Cholesterol inhibits spontaneous and oxytocin augmented uterine contractility in vitro[65, 66]
		Hypercholesterolemia activates potassium channels and may have effects on estrogen receptors and oxytocin receptors[139, 140]
	Increased required oxytocin doses	Mechanism is unknown, however BMI is not associated with oxytocin receptor gene expres- sion[141, 142]
Disruption of contraction synchronization	Irregular uterine contractions or decreased intrauterine pressure	Uterine biopsies show decreasing connexin-43 (gap junctions) mRNA in dystocia compared to normal labor[136]
		Rats with high cholesterol diet showed lower con- nexin-43 expression although contractility was not examined[66, 143]
Metabolic fatigue	Inadequate uterine contractions with poor response to oxytocin augmentation	Increased BMI is associated with excess placental ROS and decreased ATP production[58, 63, 64]

CRH corticotropin releasing hormone, BMI body mass index, mRNA messenger RNA, ATP adenosine triphosphate