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S K Lim

Publications and source records attributed to S K Lim.

111 records · Page 7Linked to original sources

Effects of long-acting somatostatin analogue (Sandostatin) on manifest diabetic ketoacidosis.

Insulin deficiency and counterregulatory hormone excess are the basic process in the development of diabetic ketoacidosis (DKA). Somatostatin, which suppresses the secretion of glucagon and growth hormone, has been known to attenuate the rate of gluconeogesis and ketogenesis in insulin-dependent diabetes mellitus patients. However, the therapeutic efficacy of somatostatin has not been approved to be practical in the treatment of manifest DKA. To examine the additive effect of octreotide, the synthetic long-acting somatostatin analogue SMS 201-995, to conventional treatment of manifest DKA, we compared the correction time of acidosis, ketonuria, and hyperglycemia of patients treated with an intravenous infusion of low-dose insulin (4 units per hour) plus subcutaneous injection of octreotide (50 microg every 6 hours) by low-dose insulin alone. The correction time for hyperglycemia and acidosis did not show any difference between groups (p = 0.089, p = 0.82). However, the time for disappearance of ketonuria of the octreotide-treated group (38.0 +/- 32.0 h) was reduced significantly compared to other group (68.3 +/- 26.0 h) (p = 0.048). These results indicated that the addition of octreotide to conventional treatment of DKA might improve the correction of ketosis, but would not allow more rapid control of acidosis and hyperglycemia in manifest DKA.

Adolescent↗

TNF-alpha and IL-6 synergistically inhibit ketogenesis from fatty acids and alpha-ketoisocaproate in isolated rat hepatocytes.

BACKGROUND: During sepsis, lipid metabolism is shunted toward triacylglycerol synthesis and hepatic lipogenesis. A decrease in ketogenesis from free fatty acids also is observed, probably mediated by cytokines involved in host response to infection. Whether such an inhibition of ketogenesis occurs with other ketone body precursors such as ketoacids is not known. The aim of this study was to determine the effects of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) on hepatic ketone body production from octanoic acid, a medium-chain fatty acid, and from alpha-ketoisocaproate (KIC), the ketoanalogue of leucine. METHODS: The experiments were conducted in cultured hepatocytes isolated from 24-hour-fasted Sprague-Dawley rats. Hepatocyte monolayers were incubated for 6 hours, with either KIC or octanoic acid (1 mmol/L), in the presence of glucagon and TNF-alpha (25 micro/L) IL-6 (15 microg/L) and/or IL-6. Acetoacetate, beta-hydroxybutyrate, and free fatty acids were determined in culture medium by enzymatic methods and KIC was measured by high-performance liquid chromatography. RESULTS: KIC and octanoic acid uptake by hepatocytes was 79% and 92%, respectively, over 6 hours, and cytokines had no influence. However, TNF-alpha and IL-6 caused inhibition of ketogenesis from alpha-ketoisocaproate (5.6% +/- 2.3% and 4.4% +/- 3.0%, respectively), and from octanoic acid (7.9% +/- 2.9%, 5.7% +/- 3.2%, respectively). In addition, when the two cytokines were present together in the culture medium, the inhibition was enhanced (inhibition of ketogenesis from KIC: 14.0% +/- 4.8%; from octanoic acid: 11.6% +/- 3.4%). CONCLUSIONS: In our experimental conditions, cytokines mediate an inhibition of ketogenesis; this process could be explained by a direct effect of cytokines on metabolic pathways of octanoic acid and KIC oran indirect effect by modification of the mitochondrial redox state.

3-Hydroxybutyric Acid↗

Comparison of propofol and methohexitone as an induction agent in anaesthesia for electroconvulsive therapy.

30 patients who received electroconvulsive therapy were anaesthetized with either Propofol or Methohexitone in a randomized cross-over study. Recovery times were shorter in those who received Propofol. The decrease in diastolic pressure after induction was greater with Propofol than with Methohexitone. There was a greater increase in the blood pressure after the electroconvulsive therapy in those who received Methohexitone. The duration of convulsion was similar for both agents.

Adolescent↗