Cancer, Ketosis and Parenteral Nutrition

Conyers, R. A. J.; Need, A. G.; Durbridge, Timothy C.; Harvey, Nathan T.; Potezny, N.; Rofe, Allan M.

doi:10.5694/j.1326-5377.1979.tb126984.x

Cited by 21 publications

(7 citation statements)

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“…Although insulin and other hormones may play a role in the above effects, it is reasonable to suggest that vasopressin may be responsible, at least in part, for the metabolic disturbances seen during sepsis. The present findings may help to explain why there is often a failure to achieve raised blood ketone-body concentrations in various other disease and injury states associated with low energy intake (Smith et Conyers et al, 1979;Rich & Wright, 1979). Time (min) Fig.…”

Section: Discussionmentioning

confidence: 71%

Metabolic effects of vasopressin infusion in the starved rat. Reversal of ketonaemia

Rofe¹,

Williamson²

1983

Biochemical Journal

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The effects of vasopressin on the metabolism of starved rats were investigated by using a constant-infusion regimen (50 pmol/kg body wt. per min, after an initial loading dose of 150 pmol/kg body wt.). 2. Blood ketone bodies decreased by 50% in 10 min, and this was accompanied by a 60% decrease in the plasma non-esterified fatty acids. 3. Blood glucose increased by 0.9 mM within 5 min and decreased to control values over the 40 min infusion. Small increases in lactate and pyruvate also occurred. 4. Plasma insulin was not increased by vasopressin infusion. 5. The net decrease in blood ketone bodies caused by vasopressin was similar when somatostatin was infused simultaneously (1 nmol/kg body wt. per min). 6. Hepatic ketone bodies were significantly decreased by vasopressin, as was the 3-hydroxybutyrate/acetoacetate ratio. A small increase in the hepatic concentration of several glycolytic intermediates also occurred. 7. Vasopressin did not decrease the ketonaemia produced by infusions of octanoate or long-chain triacylglycerol in rats that had been pre-treated with the anti-lipolytic agent 3,5-dimethylpyrazole. 8. In comparison with vasopressin, the infusion of adrenaline or glucose had much smaller effects in decreasing the ketonaemia of starvation, despite the 4-fold increase in plasma insulin, at 10 min, with the glucose infusion. 9. The primary metabolic effect of vasopressin in the starved rat appears to be that of decreased supply of non-esterified fatty acid to the liver. It is suggested that vasopressin has a direct anti-lipolytic effect in adipose tissue.

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Section: Discussionmentioning

confidence: 71%

Metabolic effects of vasopressin infusion in the starved rat. Reversal of ketonaemia

Rofe¹,

Williamson²

1983

Biochemical Journal

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“…It has been suggested that cancerous cells have an intrinsic dependence on glycolysis. The induction of ketosis (the production of ketone bodies), may reduce malignant cell growth [ 23 - 26 ]. In a 1979 study, Magee, et al studied 36 C57BL/6 mice in two different environments; one in which half the mice were fed water and sucrose (Group 1), and another where mice were only fed water and polyunsaturated, blended vegetable oil (Group 2).…”

Section: Reviewmentioning

confidence: 99%

The Efficacy of Ketogenic Diet and Associated Hypoglycemia as an Adjuvant Therapy for High-Grade Gliomas: A Review of the Literature

Varshneya¹,

Carico²,

Ortega³

et al. 2015

Cureus

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Background: A high-fat, low-carbohydrate diet, often referred to as a ketogenic diet (KD), has been suggested to reduce frequency and severity of chronic pediatric and adult seizures. A hypoglycemic state, perpetuated by administration of a KD, has been hypothesized as a potential aid to the current standard treatments of high-grade gliomas.Methods: To understand the effectiveness of the ketogenic diet as a therapy for malignant gliomas, studies analyzing components of a KD were reviewed. Both preclinical and clinical studies were included. The keywords “ketogenic diet, GBM, malignant glioma, hyperglycemia, hypoglycemia” were utilized to search for both abstracts and full articles in English. Overall, 39 articles were found and included in this review.Results: Studies in animal models showed that a KD is able to control tumor growth and increase overall survival. Other pre-clinical studies have suggested that a KD sustains an environment in which tumors respond better to standard treatments, such as chemoradiation. In human cohorts, the KD was well tolerated. Quality of life was improved, compared to a standard, non-calorie or carbohydrate restricted diet. Hyperglycemia was independently associated with diminished survival.Conclusion: Recent clinical findings have demonstrated that induced hypoglycemia and ketogenic diet are tolerable and can potentially be an adjuvant to standard treatments, such as surgery and chemoradiation. Other findings have advocated for KD as a malignant cell growth inhibitor, and indicate that further studies analyzing larger cohorts of GBM patients treated with a KD are needed to determine the breadth of impact a KD can have on GBM treatment.

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“…Moreover, it has been suggested that the in vitro growth rate of certain tumour cell lines may be reduced by the presence of 3-hydroxybutyrate at a concentration which is observed in simple starvation (Magee et al 1979). Thus, the induction of systemic ketosis in the cancer-bearing host has been suggested as a method of selectively feeding the host while restricting the supply of glucose to the tumour and reducing tumour growth rate (Conyers et al 1979;Williams & Matthaei, 1981;Tisdale, 1982).…”

Section: Dietary M a N I P U L A T I O N Of Tumour Growthmentioning

confidence: 99%