Fuel metabolism in starvation.

By G. Cahill. Annual review of nutrition, 2006

1,202 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Physiology

View Paper: https://www.semanticscholar.org/paper/a8bb8327226d35259e68ecd8edcc17a3a1380f4a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

1. P. Crawford
2. Judith Y. Altarejos
3. Patrycja Puchalska
4. M. Montminy

In Physiology

1. P. Crawford
2. Judith Y. Altarejos
3. Patrycja Puchalska
4. M. Montminy
5. M. Saitoe
6. Yukinori Hirano

Citations in the corpus

• CREB and the CRTC co-activators: sensors for hormonal and metabolic signals (2011, background): “They also increase the levels of hepatic glycogenolysis and gluconeogenesis to provide fuel for glucose-dependent tissues, such as the brain and the red blood cell compartment, which lack the enzymes required to burn free fatty acid”
• BRAIN FUEL METABOLISM, AGING AND ALZHEIMER’S DISEASE (2010, background): “Whether the third ketone, acetone, contributes directly to the brain’s energy requirements is unknown but, during prolonged fasting or starvation, up to ~60% of the human brain’s energy requirements can be met by a combination of acetoacetate and β-hydroxybutyrate [141].”
• β-Hydroxybutyrate (2017, neutral): “In humans, serum levels of BHB are usually in the low micromolar range but begin to rise to a few hundred micromolar after 12−-16 h of fasting, reaching 1−-2 mM after 2 days of fasting (13, 109) and 6−-8 mM with prolonged starvation (12).”
• Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics (2017, background): “…approximately 100 and 250 mM, rise to 1 mM after prolonged exercise or 24 hr of fasting, and can accumulate to as high as 20mM in pathological states like diabetic ketoacidosis (Cahill, 2006; Johnson et al., 1969b; Koeslag et al., 1980; Robinson and Williamson, 1980; Wildenhoff et al., 1974).”
• Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 (GPR41) (2011, background): “Ketone bodies increase dramatically in diabetes (10).”