Mitochondrial function after acute alteration of the endogenous insulin-to-glucagon ratio

Aprille, June R.; Rohweder-Dunn, Gitta; Brennan, William A.; Kelley, Richard T.; Nosek, Michael T.

doi:10.1016/0006-291x(87)90275-0

Cited by 9 publications

(3 citation statements)

References 40 publications

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“…Mitochondria isolated from hepatocytes stimulated with glucagon and Ca 2ϩ mobilizing agents such as vasopressin, thapsigargin, or Ca 2ϩ ionophores have increased AdN content (17,59,152,156,357,362,389), which is not due to an increase in mitochondrial volume (108). Glucagon-induced Ca 2ϩ signals are transient and much smaller than those elicited by ␣-adrenergic agonists (phenylephrine) or vasopressin (82,121,368), but by increasing the intracellular concentration of cAMP and protein kinase A activity, glucagon and Ca 2ϩ mobilizing agents synergistically stimulate the net inflow of Ca 2ϩ to hepatocytes through receptor-activated Ca 2ϩ channels (9,168).…”

Section: Hormonal Regulation Of Liver Mitochondria Adn Contentmentioning

confidence: 99%

Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling

Satrústegui

Pardo²,

Arco³

2007

Physiological Reviews

239

211

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Ca(2+) signaling in mitochondria is important to tune mitochondrial function to a variety of extracellular stimuli. The main mechanism is Ca(2+) entry in mitochondria via the Ca(2+) uniporter followed by Ca(2+) activation of three dehydrogenases in the mitochondrial matrix. This results in increases in mitochondrial NADH/NAD ratios and ATP levels and increased substrate uptake by mitochondria. We review evidence gathered more than 20 years ago and recent work indicating that substrate uptake, mitochondrial NADH/NAD ratios, and ATP levels may be also activated in response to cytosolic Ca(2+) signals via a mechanism that does not require the entry of Ca(2+) in mitochondria, a mechanism depending on the activity of Ca(2+)-dependent mitochondrial carriers (CaMC). CaMCs fall into two groups, the aspartate-glutamate carriers (AGC) and the ATP-Mg/P(i) carriers, also named SCaMC (for short CaMC). The two mammalian AGCs, aralar and citrin, are members of the malate-aspartate NADH shuttle, and citrin, the liver AGC, is also a member of the urea cycle. Both types of CaMCs are activated by Ca(2+) in the intermembrane space and function together with the Ca(2+) uniporter in decoding the Ca(2+) signal into a mitochondrial response.

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Section: Hormonal Regulation Of Liver Mitochondria Adn Contentmentioning

confidence: 99%

Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling

Satrústegui

Pardo²,

Arco³

2007

Physiological Reviews

239

211

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“…Although not involved in oxidative phosphorylation, which requires adenine nucleotide exchange by the ADP/ATP carriers, adenine nucleotide accumulation in rat liver mitochondria through the ATP-Mg/Pi carrier results in a progressive increase in state 3 respiration (ADP-stimulated respiration; Asimakis and Aprille, 1980;Aprille et al, 1987;Amigo et al, 2013), perhaps by increasing the driving force of the ATP-synthase (Balaban et al, 2009;Glancy and Balaban, 2012).…”

Section: Introductionmentioning

confidence: 99%

Calcium-Regulation of Mitochondrial Respiration Maintains ATP Homeostasis and Requires ARALAR/AGC1-Malate Aspartate Shuttle in Intact Cortical Neurons

Llorente‐Folch

Rueda

Amigo

et al. 2013

Journal of Neuroscience

142

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“…Glucagon injection into fed rats may result in high glucagon and high insulin concentrations in blood, whereas mannoheptulose injection results in high glucagon and low insulin levels (Tullson & Aprille, 1986;Aprille et al, 1987). Mannoheptulose may therefore provide a more appropriate model for the study of the effects of glucagon in vivo than injection of glucagon itself.…”

Section: Isolation Of Mitochondriamentioning

confidence: 99%

Treatment of rats with glucagon or mannoheptulose increases mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase activity and decreases succinyl-CoA content in liver

Quant

Tubbs

Brand

1989

Biochemical Journal

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1. The activity of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase (EC 4.1.3.5) in extracts of rapidly frozen rat livers was doubled in animals treated in various ways to increase ketogenic flux. 2. Some 90% of the activity measured was mitochondrial, and changes in mitochondrial activity dominated changes in total enzyme activity. 3. The elevated HMG-CoA synthase activities persisted throughout the isolation of liver mitochondria. 4. Intramitochondrial succinyl-CoA content was lower in whole liver homogenates and in mitochondria isolated from animals treated with glucagon or mannoheptulose. 5. HMG-CoA synthase activity in mitochondria from both ox and rat liver was negatively correlated with intramitochondrial succinyl-CoA levels when these were manipulated artificially. Under these conditions, the differences between mitochondria from control and hormone-treated rats were abolished. 6. These findings show that glucagon can decrease intramitochondrial succinyl-CoA concentration, and that this in turn can regulate mitochondrial HMG-CoA synthase. They support the hypothesis that the formation of ketone bodies from acetyl-CoA may be regulated by the extent of succinylation of mitochondrial HMG-CoA synthase.

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Mitochondrial function after acute alteration of the endogenous insulin-to-glucagon ratio

Cited by 9 publications

References 40 publications

Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling

Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling

Calcium-Regulation of Mitochondrial Respiration Maintains ATP Homeostasis and Requires ARALAR/AGC1-Malate Aspartate Shuttle in Intact Cortical Neurons

Treatment of rats with glucagon or mannoheptulose increases mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase activity and decreases succinyl-CoA content in liver

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