Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android. Learn more here!


|Download (.pdf)|Print
ACE Angiotensin-converting enzyme
ACTH Adrenocorticotrophic hormone
ADP Adenosine diphosphate
ALS Acid-labile subunit
ATP Adenosine triphosphate
GDH Glutamate dehydrogenase
GIP Glucose-dependent insulinotropic polypeptide
GLP-1 Glucagon-like peptide 1
G-6-Pase Glucose-6-phosphatase
HbA1c Hemoglobin A1c
ICMA Immunochemiluminometric
IGF-II Insulin-like growth factor II
IGFBP3 IGF-binding protein-3
KATP ATP-sensitive potassium channel
Kir Inward rectifier potassium channel
NADH Nicotinamide adenine dinucleotide (reduced form)
NICTH Nonislet cell tumor hypoglycemia
NIPHS Noninsulinoma pancreatogenous hypoglycemic syndrome
PEPCK Phosphoenolpyruvate carboxykinase
RIA Radioimmunoassay
SSTR Somatostatin receptor
SUR Sulfonylurea receptor

Circulating plasma glucose concentrations are kept within a relatively narrow range by a complex system of interrelated neural, humoral, and cellular controls. Under the usual metabolic conditions, the central nervous system is wholly dependent on plasma glucose and counteracts declining blood glucose concentrations with a carefully programmed response. This is often associated with a sensation of hunger and, as the brain receives insufficient glucose to meet its metabolic needs (neuroglycopenia), an autonomic response is triggered to mobilize storage depots of glycogen and fat. In the postabsorptive state, hepatic glycogen reserves and gluconeogenesis from the liver and kidney directly supply the central nervous system with glucose, which is carried across the blood–brain barrier by a specific glucose transport system, while the mobilization of fatty acids from triglyceride depots provides energy for the large mass of skeletal and cardiac muscle, renal cortex, liver, and other tissues that utilize fatty acids as their basic fuel, thus sparing glucose for use by the tissues of the central nervous system.

The normal lower limit of fasting plasma glucose is typically 70 mg/dL (3.9 mmol/L). Lower values may occur during prolonged fasting, strenuous exercise, or pregnancy or may occur as a laboratory artifact. In normal men, plasma glucose does not fall below 55 mg/dL (3 mmol/L) during a 72-hour fast. However, for reasons that are not clear, normal women may experience a fall to levels as low as 30 mg/dL (1.7 mmol/L) despite a marked suppression of circulating insulin to less than 5 μU/mL. They remain asymptomatic in spite of this degree of hypoglycemia, presumably because ketogenesis is able to satisfy the energy needs of the central nervous system. Basal plasma glucose declines progressively during normal pregnancy, and hypoglycemic levels may be reached during prolonged fasting. This may be a consequence of a continuous fetal consumption of glucose and diminished availability of the gluconeogenic substrate alanine. The cause of these diminished alanine levels in pregnancy is unclear. The greatly increased glucose consumption by skeletal muscle that occurs during prolonged strenuous exercise may lead to hypoglycemia (blood glucose <45 mg/dL) despite increases in hepatic glucose production. Whether the hypoglycemia in this circumstance contributes to fatigue or other symptoms in distance runners is unknown.

In vitro consumption of glucose by blood cell elements has been reported to average 10 mg/dL/h and may give rise to laboratory values in the hypoglycemic range. ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.