Glucagon stimulation of mitochondrial respiration.

Yamazaki RK

The Journal of biological chemistry1 Oct 1975Cited by 116 (Europe PMC)

PMID240844DOI10.1016/s0021-9258(19)40904-6PepBankPUB-00240844

Publisher page PubMedAsk about this study

Summary

Acute glucagon treatment of intact rats has been found to cause a stimulation of hepatic mitochondrial respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with several NAD-linked substrates and succinate were increased significantly after hormonal treatment and isolation of mitochondria. This stimulation cannot be ascribed to a partial uncoupling effect since State 4 respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with either slightly increased or unchanged. Furthermore, rates of uncoupled respiration with these substrates were also stimulated after hormonal treatment. On the other hand, respiratory rates (State 3, 4, and uncoupled) with ascorbate-N,N,N',N'-tetramethyl-p-phenylenediamine as substrate were unaffected by glucagon treatment. The hormonally stimulated rates of respiration produced a corresponding increase in the rate of generation of high energy state as indicated in measurements of Ca2+ uptake by isolated mitochondria. Rates of Ca2+ uptake were monitored by two methods: measurement of initial rates of proton ejection following CaCl2 additions and measurement of disappearance of Ca2+ from the suspension medium using murexide as indicator in a dual wavelength spectrophotometer. A significant stimulation in the initial rate of succinate-dependent Ca2+ uptake was noted after glucagon treatment of animals and isolation of hepatic mitochondria. No effect of the hormonal treatment was seen on the extent of Ca2+ uptake or the stoichiometry of H+ ejected per Ca2+ taken up. That the hormonal effect on Ca2+ transport is at the level of the substrate-induced generation of high energy state is indicated by the observation that no effect of glucagon treatment is seen on ATP-dependent Ca2+ uptake. Glucagon-induced changes in the activities of substrate-metabolizing enzymes are considered unlikely for the following reasons: (a) previously published data showed a lack of a hormonal effect on pyruvate-metabolizing enzymes and (b) data in this study showing no effect of glucagon treatment on the activity of NAD-malate dehydrogenase as measured in mitochondrial lysates. All of these observations are consistent with either an activation of mitochondrial substrate transport and/or a stimulation of mitochondrial electron transport by glucagon treatment. Regardless of the exact mechanism involved, the effect of the hormonal treatment is to produce an increase in ATP synthetic and ion-pumping capability during a period of increased energy demand, i.e. increased gluconeogenesis.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study10

10 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Mechanism
In rats, acute glucagon treatment stimulated hepatic mitochondrial respiration measured by oxygen uptake.
In plain wordsIn rats, glucagon increased liver mitochondrial respiration measured by oxygen uptake.
Peptide
Glucagon
Outcome
IncreaseHepatic mitochondrial respiration
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
Acute glucagon treatment of intact rats has been found to cause a stimulation of hepatic mitochondrial respiration as measured by monitoring oxygen uptake polarographically.
Show in the study text Report a problemFND-0024084401
02AnimalAnimal study (in vivo)Mechanism
In rats, glucagon significantly increased hepatic mitochondrial State 3 respiration with NAD-linked substrates and succinate.
In plain wordsIn rats, glucagon increased liver mitochondrial State 3 respiration with NAD-linked substrates and succinate.
Peptide
Glucagon
Outcome
IncreaseState 3 respiration with NAD-linked substrates and succinate
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
Rates of State 3 respiration with several NAD-linked substrates and succinate were increased significantly after hormonal treatment and isolation of mitochondria.
Show in the study text Report a problemFND-0024084402
03AnimalAnimal study (in vivo)Mechanism
In rats, glucagon stimulated uncoupled hepatic mitochondrial respiration with NAD-linked substrates and succinate.
In plain wordsIn rats, glucagon increased uncoupled liver mitochondrial respiration with NAD-linked substrates and succinate.
Peptide
Glucagon
Outcome
IncreaseUncoupled respiration with NAD-linked substrates and succinate
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, rates of uncoupled respiration with these substrates were also stimulated after hormonal treatment.
1 context sentence(design, population, supporting numbers)
Summary · context
Rates of State 3 respiration with several NAD-linked substrates and succinate were increased significantly after hormonal treatment and isolation of mitochondria.
Show in the study text Report a problemFND-0024084403
04AnimalAnimal study (in vivo)Mechanism
In rats, glucagon did not affect State 3, State 4 or uncoupled mitochondrial respiration with ascorbate-TMPD substrate.
In plain wordsIn rats, glucagon did not change mitochondrial respiration with ascorbate-TMPD substrate.
Peptide
Glucagon
Outcome
No significant changeRespiration with ascorbate-TMPD substrate
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
On the other hand, respiratory rates (State 3, 4, and uncoupled) with ascorbate-N,N,N',N'-tetramethyl-p-phenylenediamine as substrate were unaffected by glucagon treatment.
Show in the study text Report a problemFND-0024084404
05AnimalAnimal study (in vivo)Mechanism
In rats, glucagon-stimulated mitochondrial respiration corresponded to increased high energy state generation measured through calcium uptake.
In plain wordsIn rats, glucagon increased mitochondrial energy generation indicated by calcium uptake measurements.
Peptide
Glucagon
Outcome
IncreaseHigh energy state generation
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
The hormonally stimulated rates of respiration produced a corresponding increase in the rate of generation of high energy state as indicated in measurements of Ca2+ uptake by isolated mitochondria.
Show in the study text Report a problemFND-0024084405
06AnimalAnimal study (in vivo)Mechanism
In rats, glucagon significantly increased the initial rate of succinate-dependent calcium uptake in hepatic mitochondria.
In plain wordsIn rats, glucagon increased the initial rate of succinate-dependent calcium uptake in liver mitochondria.
Peptide
Glucagon
Outcome
IncreaseInitial succinate-dependent calcium uptake rate
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
A significant stimulation in the initial rate of succinate-dependent Ca2+ uptake was noted after glucagon treatment of animals and isolation of hepatic mitochondria.
Show in the study text Report a problemFND-0024084406
07AnimalAnimal study (in vivo)Mechanism
In rats, glucagon did not affect the extent of hepatic mitochondrial calcium uptake.
In plain wordsIn rats, glucagon did not change the total extent of calcium uptake in liver mitochondria.
Peptide
Glucagon
Outcome
No significant changeExtent of calcium uptake
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
No effect of the hormonal treatment was seen on the extent of Ca2+ uptake or the stoichiometry of H+ ejected per Ca2+ taken up.
Show in the study text Report a problemFND-0024084407
08AnimalAnimal study (in vivo)Mechanism
In rats, glucagon did not affect the stoichiometry of protons ejected per calcium ion taken up by hepatic mitochondria.
In plain wordsIn rats, glucagon did not change the ratio of protons released to calcium taken up by liver mitochondria.
Peptide
Glucagon
Outcome
No significant changeProton-to-calcium transport stoichiometry
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
No effect of the hormonal treatment was seen on the extent of Ca2+ uptake or the stoichiometry of H+ ejected per Ca2+ taken up.
Show in the study text Report a problemFND-0024084408
09AnimalAnimal study (in vivo)Mechanism
In rats, glucagon did not affect ATP-dependent hepatic mitochondrial calcium uptake.
In plain wordsIn rats, glucagon did not change ATP-dependent calcium uptake in liver mitochondria.
Peptide
Glucagon
Outcome
No significant changeATP-dependent calcium uptake
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
That the hormonal effect on Ca2+ transport is at the level of the substrate-induced generation of high energy state is indicated by the observation that no effect of glucagon treatment is seen on ATP-dependent Ca2+ uptake.
Show in the study text Report a problemFND-0024084409
10AnimalAnimal study (in vivo)Mechanism
In rats, glucagon did not affect NAD-malate dehydrogenase activity measured in mitochondrial lysates.
In plain wordsIn rats, glucagon did not change NAD-malate dehydrogenase activity in liver mitochondrial lysates.
Peptide
Glucagon
Outcome
No significant changeNAD-malate dehydrogenase activity
Study
ratn: not reported in source
Hepatic mitochondria after intact-rat glucagon treatment
Outcome group
Mitochondrial function · Liver
Studied dose
Dose not stated
Source sentences
Summary
data in this study showing no effect of glucagon treatment on the activity of NAD-malate dehydrogenase as measured in mitochondrial lysates.
Show in the study text Report a problemFND-0024084410

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
28 Oct 2026, 02:03 UTC
Study results updated
Version 1
27 Oct 2026, 16:35 UTC
First added · source update from Europe PMC

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