Creatine and carbohydrate metabolism

Ord, Margery G.; Stocken, L. A.

doi:10.1042/bj0590272

Cited by 6 publications

(3 citation statements)

References 17 publications

(2 reference statements)

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“…However, the finding that the surgical ligation of the vasculature causes a similar degree of creatinuria and creatinaemia to the high dose cadmium suggests that the ereatine does not result from the direct effect of cadmium on creatine metabolism but is a result of testicular cell damage. Previous studies have reported that the testis does have higher levels of creatine than many other tissues (Ord and Stocken 1955), although it is present mainly as the free base (Navon et al, 1985;Nicholson et al 1989) with approximately 7% (0.79 lamole/g wet weight) being present as creatine phosphate in the rat (Lee et al 1988). Most of the creatine in the testis appears to be extracellular (Lee et al 1988) but it is present in both Sertoli cells and spermatocytes (Moore unpublished results, 1989).…”

Section: Discussionmentioning

confidence: 94%

Studies on the relationship between acute testicular damage and urinary and plasma creatine concentration

Gray¹,

Nicholson²,

Creasy³

et al. 1990

Arch Toxicol

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A single dose of cadmium chloride (3.23 mumol Cd2+/kg) causing acute testicular damage in male rats also caused significant creatinuria and creatinaemia at 48 h after dosing. Doses of cadmium which did not cause testicular necrosis did not cause creatinuria or creatinaemia. Surgical ligation of the pampiniform plexus also caused ischaemic necrosis of the testis and this was followed by significant creatinuria and creatinaemia. However, neither orchidectomy followed by a toxic dose of cadmium, orchidectomy alone nor sham operation caused significant creatinuria or creatinaemia. Cadmium dosing induced a temporary loss of body weight which was less than that caused by food restriction. Food restriction did not cause significant creatinuria but did cause significant creatinaemia. These data suggest that the creatine is derived from the damaged testis and that measurement of urinary creatine may be a useful non-invasive means of detecting acute testicular damage caused by exposure to chemicals or mechanical impairment of blood flow.

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Section: Discussionmentioning

confidence: 94%

Studies on the relationship between acute testicular damage and urinary and plasma creatine concentration

Gray¹,

Nicholson²,

Creasy³

et al. 1990

Arch Toxicol

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“…'1 12 52 53 It has been shown by the euglycaemic clamp technique that these patients show insulin resistance (Henderson A, Frank KN, Little RA (personal communication).54 This insulin resistance is not confined to carbohydrate metabolism; it may account for the increased output of creatine. 55 There is also a surprising positive relation between the urinary nitrogen loss and the plasma insulin concentration, so that insulin resistance may extend to protein metabolism.12 52 When considering the increase in urinary nitrogen excretion after injury, it is important to distinguish the later increases in output from those which are often found during the first three days. During that initial period the excess of nitrogenous compounds may include quite large amounts of 3-methylhistidine and creatinine, derived from the breakdown of muscle directly damaged by the injury.…”

Section: The Flow Phasementioning

confidence: 99%

Interpretation of the metabolic effects of trauma and sepsis.

Stoner

1987

J Clin Pathol

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By interpreting the data acquired during the examination and investigation of a patient the pathologist can make an important contribution to treatment. This interpretative role is not confined to diagnosis from surgical biopsy specimens or routine blood and urine samples. It can include the interpretation of the metabolic changes which follow trauma and accompany sepsis. These metabolic effects have been studied increasingly during the past 50 years, and there is now a considerable amount of information about the state of patients in these conditions. We should go beyond the mere description of these responses and attempt to say what they mean. Even to use the word 'responses" carries interpretative overtones, and one soon begins to seek the object of these metabolic events. To do so inevitably introduces a teleological approach to the problem but we need not be ashamed of this. Teleology was first introduced into this subject by Hunter,1 and Krebs2 has adequately defended its use for this purpose. Indeed, the furtherance of pathology would often be difficult without it.Up till now the interpretation of the metabolic response to trauma has depended on two ideas. The first, proposed by Hunter,' was that all these changes were defensive, and the second, proposed later by Cuthbertson,3 was that the response could be divided into two linked parts, an early and a late, which he called the "ebb" and "flow" phases. There is little difficulty in accepting the division of the metabolic effects of trauma into two parts, an early group of changes precipitated by the injury and lasting about a day, and a second, later group of quite different changes which reach their peak during the second week after the injury. Can these two groups of effects really be linked together; can they always be described as defensive; and while "flow" may be a useful description for the hypermetabolism and catabolism of the second phase, is "ebb", which implies depression of metabolism, such a good word for the early changes in all species? During the past few years similarities between the metabolic responses to trauma and sepsis have become apparent.4 Sepsis leads to a state that combines many of the changes of the ebb and flow phases of trauma. What light can this throw on our understanding of these events, where similar changes are produced by apparently dissimilar stimuli?Trauma and sepsis affect all tissues and metabolic pathways to some extent. Our knowledge of these changes is insufficient to be able to interpret them all; but enough is now known to attempt the interpretation of the overall changes in energy metabolism 1108 copyright.

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“…Of the phosphate esters other than ATP which have been studied in isolated diaphragm, phosphocreatine has been shown to disappear very quickly in anaerobic conditions (Walaas & Walaas, 1952) or on treatment with DNP (Sacks & Sinex, 1952). This compound has not been considered to be directly implicated in the utilization of glucose (see, however, a discussion by Sacks, 1952, andby Handler, 1952;Ord & Stocken, 1955). Further examination of the relation between sensitivity to insulin and the phosphate esters of muscle would probably throw more light on the mechanism of insulin action.…”

Section: Effect Of Insulin On Rat Diaphragm Incubated Anaerobically Imentioning

confidence: 99%

The effect of insulin on the anaerobic metabolism of rat diaphragm

Ottaway

1955

Biochemical Journal

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changes in the concentrations of nucleotides taking place on addition of ITP and AMP can be accounted for by the transphosphorylations, dephosphorylations and deamination listed in Table 2. The changes taking place on addition of ADP and IDP are approximately, but not fully, accounted for by the reactions listed in Table 14. The work reported in this paper was supported by a grant from the Rockefeller Foundation.

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Creatine and carbohydrate metabolism

Cited by 6 publications

References 17 publications

Studies on the relationship between acute testicular damage and urinary and plasma creatine concentration

Studies on the relationship between acute testicular damage and urinary and plasma creatine concentration

Interpretation of the metabolic effects of trauma and sepsis.

The effect of insulin on the anaerobic metabolism of rat diaphragm

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