Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid
Abstract. The carboxylic acid balance of perfused livers from normal and streptozotocin diabetic rats (in insulin treatment or deprived of insulin for various time intervals) was determined by measurement of FFA, lactate, pyruvate and in ketone bodies in input and output medium. In livers from fed r...
Published in: | Acta Medica Scandinavica |
---|---|
Main Authors: | , , , , |
Format: | Article in Journal/Newspaper |
Language: | English |
Published: |
Wiley
1980
|
Subjects: | |
Online Access: | http://dx.doi.org/10.1111/j.0954-6820.1980.tb12857.x https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.0954-6820.1980.tb12857.x https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.0954-6820.1980.tb12857.x |
id |
crwiley:10.1111/j.0954-6820.1980.tb12857.x |
---|---|
record_format |
openpolar |
spelling |
crwiley:10.1111/j.0954-6820.1980.tb12857.x 2024-10-13T14:06:37+00:00 Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid Sestoft, Leif Folke, Morten Gammeltoft, Steen Bartels, Paul D. Kristensen, Lars ø. 1980 http://dx.doi.org/10.1111/j.0954-6820.1980.tb12857.x https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.0954-6820.1980.tb12857.x https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.0954-6820.1980.tb12857.x en eng Wiley http://onlinelibrary.wiley.com/termsAndConditions#vor Acta Medica Scandinavica volume 208, issue S639, page 7-16 ISSN 0001-6101 journal-article 1980 crwiley https://doi.org/10.1111/j.0954-6820.1980.tb12857.x 2024-09-17T04:53:05Z Abstract. The carboxylic acid balance of perfused livers from normal and streptozotocin diabetic rats (in insulin treatment or deprived of insulin for various time intervals) was determined by measurement of FFA, lactate, pyruvate and in ketone bodies in input and output medium. In livers from fed rats of either type of treatment, the carboxylic acid balance was close to zero, and the same was true for livers from 48‐hour fasting rats after 6 hours or more of insulin deprivation. Thus, when livers were perfused with a medium containing 1 mM of lactate and of FFA, the diabetic state did not turn the liver into a state of net acid production. Addition of a high concentration of glucose to the medium inhibited the rate of ketogenesis significantly in livers from fasting diabetic animals perfused for 6 hours after discontinuation of insulin treatment. In this way a high glucose concentration caused an increased net uptake of carboxylic acid in such livers. A decrease in the liver blood flow to one‐third of the normal invariably turned livers into a state of net acid production due to ( a ) a strongly diminished uptake of lactate in livers perfused with a medium containing no glucose and ( b ) by a large net lactate production in livers perfused with 20 mM glucose. On the basis of these observations and of data from available literature it is suggested that the pathogenesis of the diabetic ketoacidosis in humans can be divided into two phases: 1) An initial phase (pH 7.4 to 7.1) distinguished by a gradually increasing accumulation of acid equivalents in the body largely caused by accumulation of the keto acids (3‐hydroxybutyrate and acetoacetate) and of non‐carbonic acid equivalents originating from the excretion in the urine of ketone bodies as bases, i.e. with sodium and potassium as the corresponding cations which ensure electroneutrality. 2) A late phase (π <7.1) distinguished by severely impaired capacity for renal excretion of acid equivalents, of an impaired capacity for respiratory compensation of the ... Article in Journal/Newspaper Carbonic acid Wiley Online Library Acta Medica Scandinavica 208 S639 7 16 |
institution |
Open Polar |
collection |
Wiley Online Library |
op_collection_id |
crwiley |
language |
English |
description |
Abstract. The carboxylic acid balance of perfused livers from normal and streptozotocin diabetic rats (in insulin treatment or deprived of insulin for various time intervals) was determined by measurement of FFA, lactate, pyruvate and in ketone bodies in input and output medium. In livers from fed rats of either type of treatment, the carboxylic acid balance was close to zero, and the same was true for livers from 48‐hour fasting rats after 6 hours or more of insulin deprivation. Thus, when livers were perfused with a medium containing 1 mM of lactate and of FFA, the diabetic state did not turn the liver into a state of net acid production. Addition of a high concentration of glucose to the medium inhibited the rate of ketogenesis significantly in livers from fasting diabetic animals perfused for 6 hours after discontinuation of insulin treatment. In this way a high glucose concentration caused an increased net uptake of carboxylic acid in such livers. A decrease in the liver blood flow to one‐third of the normal invariably turned livers into a state of net acid production due to ( a ) a strongly diminished uptake of lactate in livers perfused with a medium containing no glucose and ( b ) by a large net lactate production in livers perfused with 20 mM glucose. On the basis of these observations and of data from available literature it is suggested that the pathogenesis of the diabetic ketoacidosis in humans can be divided into two phases: 1) An initial phase (pH 7.4 to 7.1) distinguished by a gradually increasing accumulation of acid equivalents in the body largely caused by accumulation of the keto acids (3‐hydroxybutyrate and acetoacetate) and of non‐carbonic acid equivalents originating from the excretion in the urine of ketone bodies as bases, i.e. with sodium and potassium as the corresponding cations which ensure electroneutrality. 2) A late phase (π <7.1) distinguished by severely impaired capacity for renal excretion of acid equivalents, of an impaired capacity for respiratory compensation of the ... |
format |
Article in Journal/Newspaper |
author |
Sestoft, Leif Folke, Morten Gammeltoft, Steen Bartels, Paul D. Kristensen, Lars ø. |
spellingShingle |
Sestoft, Leif Folke, Morten Gammeltoft, Steen Bartels, Paul D. Kristensen, Lars ø. Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid |
author_facet |
Sestoft, Leif Folke, Morten Gammeltoft, Steen Bartels, Paul D. Kristensen, Lars ø. |
author_sort |
Sestoft, Leif |
title |
Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid |
title_short |
Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid |
title_full |
Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid |
title_fullStr |
Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid |
title_full_unstemmed |
Development of Diabetic Ketoacidosis: Some Observations on and Deductions about the Sources of Acid |
title_sort |
development of diabetic ketoacidosis: some observations on and deductions about the sources of acid |
publisher |
Wiley |
publishDate |
1980 |
url |
http://dx.doi.org/10.1111/j.0954-6820.1980.tb12857.x https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.0954-6820.1980.tb12857.x https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.0954-6820.1980.tb12857.x |
genre |
Carbonic acid |
genre_facet |
Carbonic acid |
op_source |
Acta Medica Scandinavica volume 208, issue S639, page 7-16 ISSN 0001-6101 |
op_rights |
http://onlinelibrary.wiley.com/termsAndConditions#vor |
op_doi |
https://doi.org/10.1111/j.0954-6820.1980.tb12857.x |
container_title |
Acta Medica Scandinavica |
container_volume |
208 |
container_issue |
S639 |
container_start_page |
7 |
op_container_end_page |
16 |
_version_ |
1812812815097921536 |