HPL decreases maternal insulin sensitivity, and, therefore, raises maternal blood glucose levels, whilst decreasing maternal glucose utilization, which helps ensure adequate fetal nutrition (the mother responds by pancreatic endocrine upregulation; this is thought to represent an evolutionary 'arms-race' resulting from the conflict of interest between mother and fetus). Chronic hypoglycemia leads to a rise in HPL. HPL induces lipolysis with the release of free fatty acids. With fasting and release of HPL, free fatty acids become available for the maternal organism as fuel, so that relatively more glucose can be utilized by the fetus. Also, ketones formed from free fatty acids can cross the placenta and be used by the fetus. These functions help support fetal nutrition even in the case of maternal malnutrition.