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Empagliflozin reduces blood glucose levels independently of insulin secretion by reducing glucose reabsorption in the proximal renal tubules through inhibition of sodium-glucose cotransporter 2 (SGLT2). Because SGLT2 inhibitors have a different mechanism of action to conventional antidiabetic drugs,
A 31-year old non-diabetic woman presented to our hospital with symptoms of dehydration, drowsiness, fatigue, shortness of breath and vomiting present for two consecutive days prior to admission. She had started a low carbohydrate, high fat (LCHF) diet to induce weight loss while breastfeeding her
Post-exercise ketosis is known to be suppressed by physical training and by a high carbohydrate diet. As a result it has often been presumed, but not proven, that the development of post-exercise ketosis is closely related to the glycogen content of the liver. We therefore studied the effect of 1 h
The concomitant occurrence of diabetic ketoacidosis and hyperosmolarity is reported in two children, as early symptoms of misdiagnosed type 1 diabetes mellitus. The precipitating factor for both severe metabolic abnormalities was the ingestion of a large amount of high-carbohydrate-containing
Ketoacidosis is a life threatening condition usually caused by diabetes mellitus or alcohol. In this case report we present a lactating woman who developed a severe ketoacidosis a few weeks post partum. Her nutritional status was inadequate due to illness and a diet low on carbohydrates. Five case
Sodium-glucose cotransporter-2 [SGLT2] inhibitors reduce cardiovascular events and mortality in patients with diabetes, particularly patients with established cardiovascular disease. Euglycemic diabetic ketoacidosis [euDKA], a complication of SGLT2 therapy, can be exacerbated by a low We examined whether acute and/or chronic skeletal muscle anabolism is impaired with a low-carbohydrate diet formulated to elicit ketosis (LCKD) vs. a mixed macronutrient Western diet (WD). Male Sprague-Dawley rats (9-10 wk of age, 300-325 g) were provided isoenergetic amounts of a LCKD or a WD for 6
Strict restriction of carbohydrates can induce symptomatic ketoacidosis. We herein report a 76-year-old demented woman who developed ketoacidosis after 1 month of abnormal eating behavior involving selectively eating hamburger steak (estimated carbohydrate =12.7 g/day). Laboratory tests showed
Low-carbohydrate/high-fat diets (LC-HFDs) in rodent models have been implicated with both weight loss and as a therapeutic approach to treat neurological diseases. LC-HFDs are known to induce ketosis; however, systematic studies analyzing the impact of the macronutrient composition on ketosis
Introduction: With the incredibly high incidence of Type 2 Diabetes in the current population of emergency department patients, it is critical for clinicians to understand the possible complications of the treatment of this disease. Medication like canagliflozin
BACKGROUND
Non-diabetic ketoacidosis is a rare condition which can be caused by starvation. Lack of glucose can force the body into ketogenesis causing a metabolic acidosis. As previously reported in the literature, ketoacidosis might, on rare occasions, be caused by a diet with low carbohydrate
Anecdotal evidence links the initial phase of fasting or a low-carbohydrate diet with feelings of well-being and mild euphoria. These feelings have often been attributed to ketosis, the production of ketone bodies which can replace glucose as an energy source for the brain. One of these ketone
Diabetic euglycaemic ketoacidosis is a possible adverse effect of sodium-glucose co-transporter-2 inhibitors (SGLT2i). We report a case in which the combination of SGLT2i and a strict very low-carbohydrate diet led to severe diabetic ketoacidosis in a young Caucasian man with type 2 diabetes.
To study the effect of chronic ketosis on exercise performance in endurance-trained humans, five well-trained cyclists were fed a eucaloric balanced diet (EBD) for one week providing 35-50 kcal/kg/d, 1.75 g protein/kg/d and the remainder of kilocalories as two-thirds carbohydrate (CHO) and one-third
The case of five pediatric patients who presented to the Royal Children's Hospital, Melbourne with newly diagnosed diabetes mellitus between January 2001 and September 2003 is reported. Each case was complicated by hyperosmolarity and hypernatremia and required intensive therapy. Fluid intake prior