ketosis/triglyceride

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Ketosis resistance in fibrocalculous pancreatic diabetes: II. Hepatic ketogenesis after oral medium-chain triglycerides.

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A majority of patients with fibrocalculous pancreatic diabetes (FCPD) do not become ketotic even in adverse conditions. It is not clear whether this ketosis resistance is due to reduced fatty acid release from adipose tissue or to impaired hepatic ketogenesis. We tested hepatic ketogenesis in FCPD

Pseudonormoglycemia in diabetic ketoacidosis with elevated triglycerides.

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A 24-year-old newly diagnosed male patient with diabetes presented with diabetic ketoacidosis (DKA) (pH 7.16, HCO3 6.0) and extreme hypertriglyceridemia (239.35 mmol/L). The diagnosis of DKA was delayed because of the apparent depression of the true serum glucose (to 11 mmol/L). He was treated with

Plasma triglycerides and cholesterol in diabetic ketosis.

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To better characterize the severity and course of hyperlipidemia in diabetic ketosis and ketoacidosis, we measured plasma triglyceride and cholesterol concentrations in 50 episodes in 46 adults hospitalized on a municipal hospital medical service. Moderate hypertriglyceridemia was common: 32

Hepatic triglyceride storage and ketonemia in rats fed high fat diets.

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Hepatic triglycerides and ketonemia were studied on young rats fed a carbohydrate diet C or fat diets f (22.5% fat) and F (41.5% fat) for 8-15 days. Rats were sacrificed between 9 and 11 a.m. (1) Triglycerides and ketonemia varied proportionally to the diets but triglycerides were strikingly

Relation of ketosis to metabolic changes induced by acute medium-chain triglyceride feeding in rats.

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Medium-chain triglycerides (MCT) induce ketosis in several mammalian species including man. To clarify the regulation of this metabolic alteration, we fed rats either MCT or long-chain triglyceride (corn oil) and then attempted to correlate ketosis with changes in (i) concentrations of selected

The Effect of Medium Chain Triglycerides on Time to Nutritional Ketosis and Symptoms of Keto-Induction in Healthy Adults: A Randomised Controlled Clinical Trial.

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Medium chain triglycerides (MCTs) are ketogenic and might reduce adverse effects of keto-induction and improve time to ketosis and the tolerability of very low carbohydrate diets. This study investigates whether MCT supplementation improves time to nutritional ketosis (NK), mood, and symptoms of

Medium Chain Triglycerides induce mild ketosis and may improve cognition in Alzheimer's disease. A systematic review and meta-analysis of human studies.

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The brain in Alzheimer's disease shows glucose hypometabolism but may utilize ketones for energy production. Ketone levels can potentially be boosted through oral intake of Medium Chain Triglycerides (MCTs). The aim of this meta-analysis is to investigate the effect of MCTs on

The significance of serum triglyceride changes in viral ketoacidosis and Reye's syndrome.

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Standardized ketosis in man following medium chain triglyceride ingestion.

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The effect of ketosis induced by medium chain triglycerides on intracellular pH of mouse brain.

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Mild experimental ketosis increases brain uptake of 11C-acetoacetate and 18F-fluorodeoxyglucose: a dual-tracer PET imaging study in rats.

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Brain glucose and ketone uptake was investigated in Fisher rats subjected to mild experimental ketonemia induced by a ketogenic diet (KD) or by 48 hours fasting (F). Two tracers were used, (11)C-acetoacetate ((11)C-AcAc) for ketones and (18)F-fluorodeoxyglucose for glucose, in a dual-tracer format

Carnitine palmitoyltransferase I in liver of periparturient dairy cows: effects of prepartum intake, postpartum induction of ketosis, and periparturient disorders.

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Thirty-five multiparous Holstein cows were used to determine the role of mitochondrial carnitine palmitoyltransferase I (CPT I) in liver on peripartal adaptations of fatty acid metabolism. From dry-off to parturition, cows were fed a diet at either ad libitum (n = 17) or restricted intake (RI, 80%

Substrate metabolism, hormone and cytokine levels and adipose tissue signalling in individuals with type 1 diabetes after insulin withdrawal and subsequent insulin therapy to model the initiating steps of ketoacidosis.

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Lack of insulin and infection/inflammation are the two most common causes of diabetic ketoacidosis (DKA). We used insulin withdrawal followed by insulin administration as a clinical model to define effects on substrate metabolism and to test whether increased levels of

Combined Insulin Deficiency and Endotoxin Exposure Stimulate Lipid Mobilization and Alter Adipose Tissue Signaling in an Experimental Model of Ketoacidosis in Subjects With Type 1 Diabetes: A Randomized Controlled Crossover Trial.

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Most often, diabetic ketoacidosis (DKA) in adults results from insufficient insulin administration and acute infection. DKA is assumed to release proinflammatory cytokines and stress hormones that stimulate lipolysis and ketogenesis. We tested whether this perception of DKA can be reproduced in an

Momilactone B Inhibits Ketosis In Vitro by Regulating the ANGPTL3-LPL Pathway and Inhibiting HMGCS2.

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Ketogenesis is the production of ketone bodies, which provide energy when the body lacks glucose. Under ketogenic conditions, the body switches from primarily carbohydrate to fat metabolism to maintain energy balance. However, accumulation of high levels of ketone bodies in the blood results in

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