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Ketogenic and hyperglycemia

Eric C Westman, Justin Tondt, Emily Maguire, William S Yancy
Type 2 diabetes mellitus (T2DM) has reached epidemic proportions in the modern world. For individuals affected by obesity-related T2DM, clinical studies have shown that carbohydrate restriction and weight loss can improve hyperglycemia, obesity, and T2DM. Areas covered: Reducing carbohydrate intake to a certain level, typically below 50 g per day, leads to increased ketogenesis in order to provide fuel for the body. Such low-carbohydrate, ketogenic diets were employed to treat obesity and diabetes in the 19th and early 20th centuries...
September 2018: Expert Review of Endocrinology & Metabolism
Kunal Sikder, Sanket Kumar Shukla, Neel Patel, Harpreet Singh, Khadija Rafiq
BACKGROUND/AIMS: Systemic hyperlipidemia and intracellular lipid accumulation induced by chronic high fat diet (HFD) leads to enhanced fatty acid oxidation (FAO) and ketogenesis. The present study was aimed to determine whether activation of peroxisome proliferator-activated receptor-γ (PPAR-γ) by surplus free fatty acids (FA) in hyperlipidemic condition, has a positive feedback regulation over FAO and ketogenic enzymes controlling lipotoxicity and cardiac apoptosis. METHODS: 8 weeks old C57BL/6 wild type (WT) or PPAR-γ-/- mice were challenged with 16 weeks 60% HFD to induce obesity mediated type 2 diabetes mellitus (T2DM) and diabetic cardiomyopathy...
2018: Cellular Physiology and Biochemistry
Yiguo Shen, David Kapfhamer, Angela M Minnella, Ji-Eun Kim, Seok Joon Won, Yanting Chen, Yong Huang, Ley Hian Low, Stephen M Massa, Raymond A Swanson
The innate inflammatory response contributes to secondary injury in brain trauma and other disorders. Metabolic factors such as caloric restriction, ketogenic diet, and hyperglycemia influence the inflammatory response, but how this occurs is unclear. Here, we show that glucose metabolism regulates pro-inflammatory NF-κB transcriptional activity through effects on the cytosolic NADH:NAD+ ratio and the NAD(H) sensitive transcriptional co-repressor CtBP. Reduced glucose availability reduces the NADH:NAD+ ratio, NF-κB transcriptional activity, and pro-inflammatory gene expression in macrophages and microglia...
September 22, 2017: Nature Communications
Sanket Kumar Shukla, Weijing Liu, Kunal Sikder, Sankar Addya, Amrita Sarkar, Yidong Wei, Khadija Rafiq
Diabetes increases the risk of Cardio-vascular disease (CVD). CVD is more prevalent in type 2 diabetes (T2D) than type 1 diabetes (T1D), but the mortality risk is higher in T1D than in T2D. The pathophysiology of CVD in T1D is poorly defined. To learn more about biological pathways that are potentially involved in T1D with cardiac dysfunction, we sought to identify differentially expressed genes in the T1D heart. Our study used T1D mice with severe hyperglycemia along with significant deficits in echocardiographic measurements...
July 4, 2017: Scientific Reports
Caroline E Geisler, Benjamin J Renquist
Fatty liver can be diet, endocrine, drug, virus or genetically induced. Independent of cause, hepatic lipid accumulation promotes systemic metabolic dysfunction. By acting as peroxisome proliferator-activated receptor (PPAR) ligands, hepatic non-esterified fatty acids upregulate expression of gluconeogenic, beta-oxidative, lipogenic and ketogenic genes, promoting hyperglycemia, hyperlipidemia and ketosis. The typical hormonal environment in fatty liver disease consists of hyperinsulinemia, hyperglucagonemia, hypercortisolemia, growth hormone deficiency and elevated sympathetic tone...
July 2017: Journal of Endocrinology
Catherine Crinigan, Matthew Calhoun, Karen L Sweazea
Chronic high fat feeding is correlated with diabetes and kidney disease. However, the impact of short-term high fat diets (HFD) is not well-understood. Six weeks of HFD result in indices of metabolic syndrome (increased adiposity, hyperglycemia, hyperinsulinemia, hyperlipidemia, hyperleptinemia, and impaired endothelium-dependent vasodilation) compared to rats fed on standard chow. The hypothesis was that short-term HFD would induce early signs of renal disease. Young male Sprague-Dawley rats were fed either HFD (60% fat) or standard chow (5% fat) for six weeks...
2015: Journal of Nutrition and Metabolism
Kunal Varshneya, Christine Carico, Alicia Ortega, Chirag G Patil
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...
February 2015: Curēus
Tetsuya Okuda, Asami Fukui, Naoki Morita
Abnormal modification of proteins by O-linked N-acetylglucosamine (O-GlcNAc) is known to be associated with the pathology induced by hyperglycemia. However, the dynamic mechanism of O-GlcNAc modification under hyperglycemic conditions in vivo has not been fully characterized. To understand the mechanism, we established an animal model in which the glycemic status is controlled by the diet. A mutant mouse (ob/ob) which exhibits diet-induced hyperglycemia when fed a regular chow (chow) was used to establish this model; the mice were fed a very low carbohydrate ketogenic diet (KD) to improve hyperglycemia...
November 2013: Glycoconjugate Journal
Yvan Gosmain, Mounia Heddad Masson, Jacques Philippe
Type 2 diabetes (T2D) is one of the most common diseases, affecting 5-10% of the population in most countries; the progression of its prevalence has been constant over the past 50 years in all countries worldwide, creating a major public health problem in terms of disease management and financial burden. Although the pathophysiology of T2D has been attributed for decades to insulin resistance and decreased insulin secretion, particularly in response to glucose, the contributing role of glucagon in hyperglycemia has been highlighted since the early 1970s by demonstrating its glycogenolytic, gluconeogenic and ketogenic properties...
June 2013: Journal of Diabetes
T Okuda, N Morita
OBJECTIVE: To investigate whether the improvement in hyperglycemia by dietary control influences hyperglycemia-induced pathologies in tissues of juvenile obese (ob/ob) mice. DESIGN: Five-week-old ob/ob mice were fed a very low carbohydrate ketogenic diet (KD) for 7 weeks. The blood glucose levels and body weight were monitored during this period. Biochemical parameters in the serum and tissue pathologies of the mice were analyzed at the end of the 7-week period...
2012: Nutrition & Diabetes
Jae-Hyung Chang, Susan B Gurley
Akita mice have type 1 diabetes mellitus caused by a spontaneous point mutation in the Ins2 gene which leads to misfolding of insulin, resulting in pancreatic β-cell failure. Akita mice develop pronounced and sustained hyperglycemia, high levels of albuminuria, and consistent histopathological changes, suggesting that these mice may be suitable as an experimental platform for modeling diabetic nephropathy. One key feature of diabetic kidney disease in Akita mice is that the severity of renal injury is significantly influenced by genetic background...
2012: Methods in Molecular Biology
Roxana L Aguirre Castaneda, Kenneth J Mack, Aida Lteif
Diabetic ketoacidosis (DKA) is a life-threatening condition and a major cause of morbidity and mortality in children with type 1 diabetes mellitus. The deficiency of insulin leads to metabolic decompensation, causing hyperglycemia and ketosis that resolves with the administration of insulin and fluids. However, an induced state of ketosis is the basis for the success of the ketogenic diet (KD), which is an effective therapy for children with intractable epilepsy. We report the case of a 2-year-old girl who presented to the emergency department with 1-week history of decreased activity, polyuria, and decreased oral intake...
February 2012: Pediatrics
Ghadeer Zatara, Rachel Hertz, Maayan Shaked, Nina Mayorek, Etedal Morad, Etty Grad, Amos Cahan, Haim D Danenberg, Terry G Unterman, Jacob Bar-Tana
OBJECTIVE: Overactivity of the Forkhead transcription factor FoxO1 promotes diabetic hyperglycemia, dyslipidemia, and acute-phase response, whereas suppression of FoxO1 activity by insulin may alleviate diabetes. The reported efficacy of long-chain fatty acyl (LCFA) analogs of the MEDICA series in activating AMP-activated protein kinase (AMPK) and in treating animal models of diabesity may indicate suppression of FoxO1 activity. RESEARCH DESIGN AND METHODS: The insulin-sensitizing and anti-inflammatory efficacy of a MEDICA analog has been verified in guinea pig and in human C-reactive protein (hCRP) transgenic mice, respectively...
July 2011: Diabetes
Alaa Al-Khalifa, Thazhumpal Chacko Mathew, Naji S Al-Zaid, Elizabeth Mathew, Hussein M Dashti
INTRODUCTION: Changes in dietary habits influence the glycemic level. Preliminary studies using the low-carbohydrate ketogenic diet (LCKD) were found to be quite promising in controlling diabetes mellitus. Therefore, the objectives of this study are to investigate the therapeutic effects of LCKD in experimental diabetic rats following the administration of streptozotocin (STZ). MATERIALS AND METHODS: Adult rats were divided into three groups: normal diet, LCKD, and high-carbohydrate diet...
November 2009: Nutrition
Eric S Muise, Barbara Azzolina, David W Kuo, Mohamed El-Sherbeini, Yejun Tan, Xiling Yuan, James Mu, John R Thompson, Joel P Berger, Kenny K Wong
Adipose tissue is a metabolically responsive endocrine organ that secretes a myriad of adipokines. Antidiabetic drugs such as peroxisome proliferator-activated receptor (PPAR) gamma agonists target adipose tissue gene expression and correct hyperglycemia via whole-body insulin sensitization. The mechanism by which altered gene expression in adipose tissue affects liver and muscle insulin sensitivity (and thus glucose homeostasis) is not fully understood. One possible mechanism involves the alteration in adipokine secretion, in particular the up-regulation of secreted factors that increase whole-body insulin sensitivity...
August 2008: Molecular Pharmacology
A G C Bergqvist, J I Schall, E L Richard, P R Gallagher, V A Stallings
The purpose of this study was to determine if hypoglycemia or hyperglycemia predicts the response to a ketogenic diet (KD) in a cohort of children with intractable epilepsy. We evaluated whether morning blood glucose during the initial 21 days after initiation of the KD in children with IE was related to seizure reduction after 3 months of treatment. The relation between change in weight status and blood glucose was also explored. Fasting morning whole blood glucose was measured each day for the first 21 days after initiation of KD...
August 2007: Neuropediatrics
E Renard
Use of portable pumps is increasing to achieve intensive insulin treatment. Beside unpredictable insulin absorption and insufficient reactivity to changes of insulin flow rate due to the subcutaneous route, this therapy is however limited by the lack of information on blood glucose level provided by self-blood glucose monitoring. Thus, patient interpretation only leads to speculative adaptation of pump flow rate. The lack of alert toward the risk of hypoglycemia or hyperglycemic ketogenic deviations can lead to the occurrence of deleterious metabolic distorsions, among which severe hypoglycemia stands in first rank...
April 2003: Diabetes & Metabolism
B Gumbiner, J A Wendel, M P McDermott
To determine whether high-ketogenic very-low-energy diets (VLEDs) can reduce hepatic glucose output (HGO) and hyperglycemia more effectively than can low-ketogenic VLEDs in obese patients with non-insulin-dependent diabetes mellitus (NIDDM), seven patients were treated with a high-ketogenic VLED for 3 wk and were compared with six patients treated with a low-ketogenic VLED. All patients were then crossed over and treated with the alternate diet for another 3 wk. Basal HGO, fasting ketone bodies, and glycemia, insulin, and C-peptide after fasting and an oral-glucose-tolerance test (OGTT) were measured...
January 1996: American Journal of Clinical Nutrition
A Avogaro, L Gnudi, A Valerio, A Maran, M Miola, A Opportuno, A Tiengo, D M Bier
The effects of two different plasma glucose concentrations (5 and 10 mmol/L) on lipolysis and ketogenesis during baseline and in response to epinephrine infusion were evaluated in insulin-dependent diabetic patients. Each insulin-dependent diabetic subject was studied during euglycemia, hyperglycemia with hypoinsulinemia, and hyperglycemia with hyperinsulinemia. Total ketone body (TKB) concentrations were significantly higher in hyperglycemic-hypoinsulinemic diabetics than in hyperglycemic-hyperinsulinemic and normoglycemic diabetics...
April 1993: Journal of Clinical Endocrinology and Metabolism
L Cherian, K Peek, C S Robertson, J C Goodman, R G Grossman
OBJECTIVES: Glucose is the primary substrate for the energy requirements of the nervous system. Nevertheless, administration of glucose to critically ill patients with central nervous system trauma may have adverse effects on their neurologic recovery. The purpose of this study was to evaluate the effects of other sources of nonprotein calories on spinal cord lactate accumulation and on electrophysiologic recovery after a period of severe spinal cord ischemia. DESIGN: Two randomized, blinded studies were performed: one of glycolytic energy substrates (fructose, xylitol, sorbitol, glycerol) and one of ketogenic energy substrates (beta-hydroxybutyrate, acetate, butyrate)...
November 1994: Critical Care Medicine
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