Disease relevance of Ketosis

• Elevated glycine levels in the brain and cerebrospinal fluid appear to differentiate these two forms of hyperglycinemia better than the presence of ketosis or leukopenia, and high glycine levels apparently occur in the same areas as the spongy change [1].
• The early increase of ODC activity occurred in the presence of mild hyperglycemia without ketosis or hyperglucagonemia, but the levels were much higher in severely diabetic animals [2].
• Ketone body production and disposal in diabetic ketosis. A comparison with fasting ketosis [3].
• Mild acidosis developed during the protein diet as well as greater excretions of urinary ammonium and urea N, a greater degree of ketosis, and significantly better N balance (-42.7 vs -80.4 g, p less than 0.05) than during the glucose diet [4].
• Butanediol induced ketosis increases tolerance to hypoxia in the mouse [5].

High impact information on Ketosis

• Creatinine determination in ketosis [6].
• In the diabetic subjects with ketosis in the resting state, exercise elicited a rise in arterial glucose and FFA, an augmented splanchnic uptake of FFA, and a 2-3 fold increase in splanchnic output of 3-hydroxybutyrate [7].
• In the three of the six patients who developed significant ketosis, plasma-glucagon showed a close correlation with blood-ketones and plasma-free-fatty-acids while for the whole group the change in glucagon concentration correlated significantly with the rise in ketone-body concentration [8].
• This study examined the hypothesis that ketosis increases the TNF-alpha secretion, both in a cell culture model using U937 monocytes and in type 1 diabetic patients in vivo [9].
• Lethal hypoglycemic ketosis and glyceroluria in mice lacking both the mitochondrial and the cytosolic glycerol phosphate dehydrogenases [10].

Chemical compound and disease context of Ketosis

• Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L [11].
• Maternal-fetal carnitine relationship and neonatal ketosis in the rat [12].
• PORH was similar in baseline conditions, during ketosis, and in recovery in both the placebo and INDO arms [13].
• Persistence of ketosis despite suppression of lipolysis by 16,16-dimethylprostaglandin E2 in experimental diabetic ketoacidosis in rats [14].
• The observation that the ester fraction in the newly synthesized plasma carnitine increased with fasting (84.0 versus 67.9%) indicates that the surplus plasma acylcarnitine in fasting ketosis derives from the liver [15].

Biological context of Ketosis

• There was a significant correlation (r = 0.36, P < 0.05; n = 34) between ketosis and oxidative stress as well as between oxidative stress and TNF-alpha levels (r = 0.47, P < 0.02; n = 34) in the blood of diabetic patients [9].
• Pregnancy induces complex changes in energy metabolism, manifested clinically by insulin resistance, low fasting blood glucose levels, and proneness to ketosis [16].
• 1. The aim of this study was to determine the effect of a constant infusion of glucose on the ketosis that is observed when dairy cows are deprived of food in early lactation [17].
• We hypothesized based on these findings that ketosis resulting from KD might inhibit glutamate cytotoxicity, resulting in inhibition of hippocampal neuronal cell death [18].
• From d 14 to 42 postpartum, 13 Holstein cows were in either a control group (6 cows) or a ketosis induction group (7 cows) that was restricted to 80% of ad libitum intake and fed 1,3-butanediol (7% of DM) [19].

Anatomical context of Ketosis

• Tissue sensitivity to insulin (euglycemic insulin clamp technique), hepatic glucose production (3-[3H]glucose infusion) and insulin binding to erythrocyte receptors were studied in 14 newly diagnosed type 1 diabetic patients after the disappearance of ketosis and after 3 months of insulin therapy [20].
• The authors report the measurement of brain BHB and lactate in the occipital lobe of healthy adults using high field (4-T) magnetic resonance spectroscopy, measured in the nonfasted state and after 2- and 3-day fasting-induced ketosis [21].
• Thus the term "energy associated disease" was created to assess the combined impact of the precalving monensin treatment on the incidence of retained placenta, displaced abomasum, and clinical ketosis [22].
• Stimulation of ketogenesis by propionate in isolated rat hepatocytes: an explanation for ketosis associated with propionic acidaemia and methylmalonic acidaemia [23]?
• Twelve percent of these cows had subclinical ketosis, defined as >1400 micromol of beta-hydroxybutyrate/L of blood serum [24].

Gene context of Ketosis

• Effects of somatostatin on established induced ketosis [25].
• There was a significant correlation between ketosis and IL-6 levels (r = 0.36, P < 0.04, n = 34) in the blood of diabetic patients [26].
• Specifically, alpha-synuclein rescued cells from MPP+ mediated decreases in mitochondrial dehydrogenase activity and loss of ATP levels by utilizing ketosis [27].
• Patients homozygous for the T435N mutation of succinyl-CoA:3-ketoacid CoA Transferase (SCOT) do not show permanent ketosis [28].
• High glucagon is said to be necessary for ketosis in severe forms of diabetes [29].

Analytical, diagnostic and therapeutic context of Ketosis

• As an indicator of ketosis in epilepsy patients consuming a ketogenic diet, breath acetone may be useful for understanding the mechanism of the diet, elucidating the importance of ketosis in seizure protection, and ultimately, enhancing the efficacy of the diet by improving patient monitoring [30].
• CONCLUSIONS: Ketosis during hepatectomy was caused by increased beta-hydroxybutyrate, and this phenomenon was observed only in patients with seriously impaired liver function [31].
• After treatment for ketosis, glucose and insulin concentrations of plasma were greater than prepartal concentrations [32].
• Previously, it was difficult to maintain ketosis when parenteral (iv) nutrition therapy was necessary [33].
• Ketosis leads to increased methylglyoxal production on the Atkins diet [34].

References