Ketogenesis and their utilization is taking place even in normal conditions but both process occur at slow level in such a way that their normal level remains <1.0 mg/dl. Dr. Inayat u Rahman Abbasi 5 6. KB concentration when increased in body indicates: Excessive production acetyl CoA (increased Lipolysis) or Depressed utilization of acetyl CoA. Ketogenesis 1. Acetyl-CoA synthesised from fatty acids can enter and get oxidised in TCA cycle only when carbohydrates are available. During starvation and diabetes mellitus, acetyl-coA takes a different route of formation of ketone bodies. 2 World's Best PowerPoint Templates - CrystalGraphics offers more PowerPoint templates than anyone else in the world, with over 4 million to choose from. Winner of the Standing Ovation Award for Best PowerPoint Templates from Presentations Magazine. They'll give your presentations a professional, memorable appearance - the kind of sophisticated look that today's audiences expect
. 24.4 Ketogenesis and Ketone Bodies The accumulation of ketone bodies may lead to a condition called ketosis, which occurs in cases of severe diabetes, diets high in fat and low in carbohydrates, alcoholism, and starvation. A ketone test strip indicates the level of ketone bodies in a urine sample View Ketogenesis PPTs online, safely and virus-free! Many are downloadable. Learn new and interesting things. Get ideas for your own presentations. Share yours for free Ketogenesis takes place in mitochondria of liver using Acetyl co A as a substrate or a precursor molecule. Enzymes responsible for ketone body formation are associated mainly with the mitochondria HMG co A synthase is the rate limiting enzyme 5. This enzyme is exclusively present in liver mitochondria REGULAITION OF KETOGENESIS • Ketogenesis is regulated mainly by: 1. Substrate availability • Increased ketogenesis occurs when there is excessive availability of fatty acids for oxidation. Thus, increased ketogenesis occurs during starvation or diabetes mellitus. 2. Regulation of β-oxidation • Increased glucagon and decrease insulin in.
Ketogenesis is a very important physiological process. It is exclusively hepatic. The regulation of ketogenesis depends mainly on the concentration of 2 hormones: insulin and glucagon. In mammals a decrease in blood glucose concentration depresses insulin and increases glucagon View 12-Ketone bodies.ppt from BIOLOGY 201L at Northern Arizona University. Ketone Bodies Dr.Haidar Almamari Metabolism of Ketone Bodies It includes: 1.Ketogenesis , synthesis of ketone bodies i Ketogenesis is the biochemical process through which organisms produce ketone bodies by breaking down fatty acids and ketogenic amino acids. The process supplies energy to certain organs, particularly the brain, heart and skeletal muscle, under specific scenarios including fasting, caloric restriction, sleep, or others
Pathogenic links between diets and particular oncogenes remain unknown. Xia et al. demonstrate that a high-fat diet increases circulating acetoacetate that enhances tumor growth potential of BRAF V600E melanoma cells in mice, which informs the design of a precision diet to lower cancer risk and development of metabolism-targeted therapies for cancer treatment . In the liver, control of ketogenesis is largely due to the blocking of other pathways in the metabolism of the carbon product of fatty acid oxidation, acetyl-CoA (oxidation and fat synthesis). The ketoacids formed become the main fuel for the brain 24.4 Ketogenesis And Ketone Bodies PPT Presentation Summary : The accumulation of ketone bodies may lead to a condition called ketosis, which occurs in cases of severe diabetes, diets high in fat and low in carbohydrates
Regulation Of Ketogenesis, Ketogenesis Pathway, Ketone Body, Ketogenesis and Ketolysis, Production of Ketone Bodies, Formation of Ketone Bodies, Liver Ketogenesis, Fatty Acid Breakdown, Ketosis Mechanism, Ketone Metabolism, Ketosis Cycle, Ketone Bodies Synthesis, Types of Ketone Bodies, Ketosis Metabolic Pathway, Ketone Body Utilization, acetyl-CoA to Ketone, Starvation Biochemistry, Lipid. Ketogenesis (1, 2) is a biochemical process that produces ketone bodies by breaking down fatty acids and ketogenic amino acids. The process supplies the needed energy of certain organs, especially the brain. Not having enough ketogenesis could result to hypoglycaemia and over production of ketone bodies leading to a condition called ketoacidosis fatty acids are mobilized for β-oxidation and ketogenesis. Glucocorticoids and thyroid hormones act on nuclear hormone receptors to activate transcription. DNA binding by thyroid hormone receptors. Thyroid hormones induce respiratory chain uncoupling proteins. PowerPoint Presentation Last modified by
Ketones and Aldehydes Properties Nomenclature Preparation Reactions Synthesis Imines and Enamines Imine Derivatives Wolff-Kishner Reduction Mechanism from Hydrazone Deoxygenation Enamine Mechanism (same as imine mech. until last step) Wittig Reaction: C=O into C=C Ylide Synthesis Mechanism Pure Alkene is Formed in Wittig Rxn (Methoxymethylene)-triphenylphosphorane an Aldehyde Prep Propose a. WHAT IS KETOGENESIS Ketogenesis is a catabolic pathway of metabolism. In this process, fatty acids and certain ketogenic amino acids are broken down to derive energy by alternative means. Ketone bodies are produced in the ketogenesis process. Our body continuously produces ketone bodies in low amounts but in certain cases like starving, whe Ketogenesis is the process by which fatty acids are transformed into AcAc and 3HB. This process takes place in the mitochondria of perivenous hepatocytes 20 - 23. The production of fatty acids and their conversion to fuel or to ketone bodies are determined by several factors (Figure 2) . However, this process occurs in a reverse manner while fasting. The initial defense mechanism in response to decreased glucose level is the reduction of insulin
View Chapter 5 Lipids-1.ppt from BIOCHEMIST 103 at DaLi University. Chapter 5 Metabolism of Lipids Introduction • Lipids are substances that are insoluble in water, but soluble in organic • Ketogenesis occurs only in liver because the enzymes synthesizing ketone body exist in liver 6 Laboratory Features Diagnostic for DKA • Serum glucose > 250 mg/dL (13 9Serum glucose > 250 mg/dL (13.9 mmol/L) • Arterial pH < 7.35 (venous pH <7.3) • Serum bicarbonate < 18 mEq/L • Serum acetone test positive • Urinary ketone test positive (3+) Additional Laboratory Features Consistent with DKA • WBC count elevated (but < 25 000/mmWBC count elevated (but < 25,000/mm3 ADVERTISEMENTS: In this article we will discuss about:- 1. Formation of Ketone Bodies 2. Conditions Leading to Ketosis 3. Source 4. Utilisation 5. Interrelation with Carbohydrate Metabolism 6. Ratio 7. Relation of Ketosis with Blood and Urine Reaction 8. Role of Endocrine. Formation of Ketone Bodies (Ketogenesis): It has been observed that acetyl CoA produced [
Save figures into PowerPoint; Download tables as PDFs; Go to My Dashboard Close. Defects in ketone body synthesis (ketogenesis) result in hypoketotic hypoglycemic crises during prolonged fasting or febrile illness, whereas defects in ketone body utilization (ketolysis) result in ketoacidotic crises. While both acetoacetate and 3. Ketones - Compounds That Have A Carbonyl Group Bonded To PPT Presentation Summary : Ketones. Ketones - compounds that have a carbonyl group bonded to two carbons. So, both aldehydes and ketone contain a carbonyl group Metabolism of lipids.ppt - Free download as Powerpoint Presentation (.ppt), PDF File (.pdf), Text File (.txt) or view presentation slides online. Scribd is the world's largest social reading and publishing site. Ketogenesis The ketone bodies are acetoacetate bhydroxybutyrate acetone Ketogenesis is the process by which ketone bodies ar
Ketogenesis. If excessive acetyl CoA is created from the oxidation of fatty acids and the Krebs cycle is overloaded and cannot handle it, the acetyl CoA is diverted to create ketone bodies. These ketone bodies can serve as a fuel source if glucose levels are too low in the body. Ketones serve as fuel in times of prolonged starvation or when. • Ketogenesis • Sintesis HDL. 2/11/2015 50 Ketogenesis. 2/11/2015 51 KETOGENESIS =Proses pembentukan senyawa keton di dalam tubuh, terdiri dari :-Asetoasetat-β-Hidroksi butirat-Aseton • Tempat sintesis : Hati • Ketosis Ketonuria Ketonemia. 2/11/2015 52 Asam lemak hati berasal dari The consequences of Hormones! , Low/No Insulin leads to biochemical stress, observed by increased in counter-regulatory hormones, such as: - Glucagon, Cortisol, GH, Epinephrine , Glucagon does the following: 1) Stimulates hepatic gluconeogenesis (utilizes glycerol and alanine) 2) Stimulates ketogenesis at mitochondria (of FFAs into ketone bodies leading to hyperketonaemia, usually inhibited by.
The overall rate of hepatic ketogenesis may by affected by several factors: 1. Control in the release of free fatty acids from adipose tissue directly affects the level of ketogenesis in the liver. This is, of course, substrate-level regulation. Fatty acid release from adipose tissue is controlled via the activity of hormone-sensitive lipase (HSL) #### What you should know Diabetic ketoacidosis (DKA) is an extreme metabolic state caused by insulin deficiency. The breakdown of fatty acids (lipolysis) produces ketone bodies (ketogenesis), which are acidic. Acidosis occurs when ketone levels exceed the body's buffering capacity (figure⇓).1 2 Diabetic ketoacidosis may follow absolute insulin deficiency or relative insulin deficiency Ketone bodies, or simply ketones are substances produced by the liver during gluconeogenesis, a process which creates glucose in times of fasting and starvation. There are three ketone bodies produced by the liver. They are acetoacetate, beta-hydroxybutyrate, and acetone
SGLT2 inhibitors have been shown to offer potent renoprotection against diabetic kidney disease. But the mechanism for this effect has been unclear. Here, Tomita et al. report that the drugs promote elevation of ketone bodies, which subsequently inhibit mTORC1 in the proximal renal tubules, explaining their protective effects on this organ View glucose metabolism.ppt from BCH 3701 at University of South Africa. and and gluconeogenesis lypolisis lypolisis lypolisis lypolisisand and lypolisis lypolisis lypolisis and ketogenesis ketogenesis lypolisis ketogenesis ketogenesis ketogenesis diabetes mellitus pathogenesis A B S O L U T E /R E L A T I V E L A C K O F IN S U L IN H Y P. Background: RPE cells derive fatty acids from phagocytized photoreceptor outer segments.Results: RPE cells metabolize palmitate to produce β-hydroxybutyrate (β-HB), a ketone body the retina can use as a metabolic substrate.Conclusion: RPE cells produce β-HB as a potential substrate for photoreceptor cells in the outer retina.Significance: This is a novel form of RPE-retina interaction that. Ketogenic amino acids are amino acids that can be converted into ketone bodies through ketogenesis. Pages in category Ketogenic amino acids The following 8 pages are in this category, out of 8 total. This list may not reflect recent changes.
- ketogenesis - triacylglycerol synthesis อ. ชัยวัฒน์ วามวรรัตน์ citrate-malate-pyruvate shuttle citrate-malate-pyruvate shuttle formation of malonyl-coa eukaryotic acc powerpoint presentation fatty acid synthase fatty acid biosynthesis 1. loading 3. reduction 4.dehydration 5.reduction condensation step. Ketogenesis is a metabolic process leading to the production of ketone bodies—acetoacetate, beta‐hydroxybutyrate, acetone—an alternative fat‐derived metabolic fuel for vital organs in states of nutrient deprivation, such as fasting, glucose deprivation, and prolonged physical exercise. Open in figure viewer PowerPoint We investigated the interrelations between C4 ketogenesis (production of β-hydroxybutyrate + acetoacetate), C5 ketogenesis (production of β-hydroxypentanoate + β-ketopentanoate), and anaplerosis in isolated rat livers perfused with 13C-labeled octanoate, heptanoate, or propionate. Mass isotopomer analysis of C4 and C5 ketone bodies and of related acyl-CoA esters reveal that C4 and C5. Start studying Fatty Acid Oxidation and Ketogenesis: Biochemistry. Learn vocabulary, terms, and more with flashcards, games, and other study tools
GENERAL. ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis INTRODUCTION. Hepatocytes acutely produce ketones to spare glucose utilization during a fast, when insulin signaling is low and hepatic lipid oxidation is dominant ().Yet, with the rise in nonalcoholic fatty liver disease (NAFLD) and the adoption of ketogenic diets, ketosis is a prolonged metabolic state for many individuals NUT 202-BIOCHEMISTRY of WELL-FED STATE and STARVATION.ppt - Prof Dr Nedret KILI\u00c7 Integration of Metabolism 1 Interconnection of pathways 2 Metabolic (glycerol, muscle proteins) • ketogenesis (storage TAG → FFA → ketone bodies) The figure was adopted from Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations. Dka Case Presentation Ppt . Dec 26, 2017 DTN Staff. twitter. pinterest. facebook. Impaired peripheral glucose utilization resulting in hyperosmolarity and hyperglycemia Increased lipolysis and ketogenesis resulting in metabolic acidosis and ketonemia Hyperglycemia exceeding the renal threshold and hyperketonemia cause the osmotic diuresis,. Previously, we demonstrated that mitochondrial bioenergetic deficits preceded Alzheimer's disease (AD) pathology in the female triple-transgenic AD (3xTgAD) mouse model. In parallel, 3xTgAD mice exhibited elevated expression of ketogenic markers, indicating a compensatory mechanism for energy production in brain. This compensatory response to generate an alternative fuel source was temporary.
Daily, the retinal pigment epithelium (RPE) ingests a bolus of lipid and protein in the form of phagocytized photoreceptor outer segments (OS). The RPE, like the liver, expresses enzymes required for fatty acid oxidation and ketogenesis. This suggests that these pathways play a role in the disposal of lipids from ingested OS, as well as providing a mechanism for recycling metabolic. Start studying 4. Fatty Acid Oxidation (PPT). Learn vocabulary, terms, and more with flashcards, games, and other study tools Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific fruity smell. Onset of symptoms is usually rapid.. Accumulating acetyl-CoA is shunted through ketogenesis to produce the ketone bodies acetoacetate and β-hydroxybutyrate. These substrates, which are water-soluble forms of fat, are metabolized to acetyl-CoA and used for energy production by many tissues (e.g., muscle, brain, kidney) but not by red blood cells or the liver Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria.It occurs when absolute or relative insulin deficiency inhibits the ability of glucose to enter cells for utilization as metabolic fuel, the result being that the liver rapidly breaks down fat into ketones to employ as a fuel source
Ketogenesis is a highly integrated process that comprises a number of potential pace‐setting steps (19; 53; 12). Recent determination of flux control coefficients of the enzymes involved in ketogenesis shows that CPT‐I catalyzes the pace‐setting step of ketogenesis from long‐chain fatty acids in both hepatocytes ( 11 ; 36 ) and. Diabetes Mellitus - Biochemistry. 1. Diabetes mellitus is the 3rd leading cause of death in many developed countries. Diabetes is a major cause of blindness, renal failure, amputation, heart attacks and stroke. Diabetes mellitus is a characterized by increased blood glucose level (hyperglycemia) due to insufficient or inefficient (incompetent) insulin Intestinal ketogenesis, induced by prolonged high-fat feeding, may be a mechanism blunting GLP-1 responsiveness in obese subjects before surgery. After gastric bypass-surgery, this mechanism may be relieved by the inhibition of intestinal ketogenesis, promoting the rapid improvement of the GLP-1 response after surgery The Western diet is rich in salt, and a high salt diet (HSD) is suspected to be a risk factor for cardiovascular diseases. It is now widely accepted that an experimental HSD can stimulate components of the immune system, potentially exacerbating certain autoimmune diseases, or alternatively, improving defenses against certain infections, such as cutaneous leishmaniasis. However, recent.
View lipidmetabolism.l F.ppt from ZOO 101 at Quaid-i-Azam University, Islamabad. Lipid Metabolism 1 Fatty Acids CH3(CH2)nCH2C Reduction of total daily insulin dose may cause failure to suppress lipolysis and ketogenesis . Association with increase in glucagon. Reduction in renal clearance of ketone bodies. Danne et al. Diabetes Care 2019;42(6):1147-54. SGLT-inhibitors are associated with an increase in glucagon, perhaps as a result of urinary glucose loss or throug ketogenesis Unique combination of hypoglycaemia + suppression of ketogenesis → no fuel source for brain ANY detectable insulin (>2microU/ml) in the presence of a BGL <2.6mmol/l is inappropriate Aim of treatment is BGL >4.0mmol/l Insulin secretion - mechanism The beta cell functions to transform the chemica
METABOLIC CHANGES IN DIABETES MELLITUS.pptx - Free download as Powerpoint Presentation (.ppt / .pptx), PDF File (.pdf), Text File (.txt) or view presentation slides online. Scribd is the world's largest social reading and publishing site Ketone bodies are water-soluble molecules that contain the ketone groups produced from fatty acids by the liver (ketogenesis). They are readily transported into tissues outside the liver, where they are converted into acetyl-CoA (acetyl-Coenzyme A)—which then enters the citric acid cycle (Kreb's cycle) and is oxidized for energy. Ketone bodies in the brain are used to convert acetyl-CoA into.
The flux-generating step in ketogenesis appears to be lipolysis of TG in adipocytes. Ketone bodies stimulate modest insulin release, and they also feedback negatively on hormone sensitive lipase (HSL) activity in adipocytes. Ketone bodies are preferred fuel in the brain during starvation. AcAc and b-OH-butyrate can be used in the biosynthesis. One symptom of ketogenesis is that the patient's breath smells sweet like alcohol. This effect provides one way of telling if a diabetic is properly controlling the disease. The carbon dioxide produced can acidify the blood, leading to diabetic ketoacidosis, a dangerous condition in diabetics important role in the control of ketogenesis (Brindle et al.. 1985; Jesse et al., 1986a, 1986b). The flux generating step for ketone production is the, release of free fatty acids from. The decline in Bifidobacterium abundance was associated with the induction of ketogenesis and not the complete lack of CHO, providing additional support for the importance of ketone bodies. However, we also observed low Bifidobacterium levels in mice fed a low-fat, high-plant-polysaccharide chow diet, warranting additional studies
Glucagon is a peptide hormone, produced by alpha cells of the pancreas.It raises concentration of glucose and fatty acids in the bloodstream, and is considered to be the main catabolic hormone of the body. It is also used as a medication to treat a number of health conditions. Its effect is opposite to that of insulin, which lowers extracellular glucose. It is produced from proglucagon. Welcome to Shomu's Biology - Simplifying life sciences for future biologists Shomu's Biology is created keeping a goal in mind that every single one of us deserve a better understanding of biological science explained in a simple manner no matter how difficult the topics are Ketogenesis occurs in the liver and depends on the transcription factor PPARalpha, as demonstrated by the severely impaired ketogenesis in mice with a germline deletion of the Ppara gene (Kersten et al., 199 We have measured rates of ketogenesis and malonyl-CoA contents of hepatocytes isolated from meal-fed rats under a variety of incubation conditions in order to determine the relationship between the intracellular malonyl-CoA level and the rate of ketogenesis. Evidence obtained from rat liver homogenates suggested that malonyl-CoA, which is a major determinant of fatty acid synthesis in vivo.
Regulation of Ketogenesis: a. In adipose tissue, very high concentrations of plasma-free fatty acids (FFA) are available as a result of lipolysis of triacylglycerol. In fed as well as in fasting conditions, 30% or more of the free fatty acids pass to the liver 08.Metabolic Response to Trauma.ppt - Free download as Powerpoint Presentation (.ppt), PDF File (.pdf), Text File (.txt) or view presentation slides online. 08.Metabolic Response to Trauma.ppt Physiology of Starvation - Free download as Powerpoint Presentation (.ppt / .pptx), PDF File (.pdf), Text File (.txt) or view presentation slides online. Scribd is the world's largest social reading and publishing site. As FFA level increase, ketogenesis is stimulated and ketone bodies are formed In patients with type 2 diabetes, a right‐shifted dose-response curve for insulin vs. ketogenesis has been reported, suggesting resistance on insulin‐mediated suppression of ketogenesis (). The present study was designed to investigate KB metabolism (i.e., TKB Ra ) in obese insulin‐resistant subjects after 38 h of fasting in relation to.
Recently, the U.S. Food and Drug Administration (FDA) issued a Drug Safety Communication that warns of an increased risk of diabetic ketoacidosis (DKA) with uncharacteristically mild to moderate glucose elevations (euglycemic DKA [euDKA]) associated with the use of all the approved sodium-glucose cotransporter 2 (SGLT2) inhibitors (1). This Communication was based on 20 clinical cases. LIPID METABOLISM- ketogenesis: LIPID METABOLISM- ketogenesis Dr. Hariharan , V Assistant professor, Department of Biochemistry, Karpagam Faculty of Medical Sciences and Research, Coimbatore
Ketogenesis. If excessive acetyl CoA is created from the oxidation of fatty acids and the Krebs cycle is overloaded and cannot handle it, the acetyl CoA is diverted to create ketone bodies.These ketone bodies can serve as a fuel source if glucose levels are too low in the body The metabolic pathways are complex and interdependent. With the changing environments the reactions of metabolism must be finely regulated to maintain a constant set of conditions within cells, a. Ketogenesis. Ketogenesis takes place in the liver using Acetyl co A as a substrate or a precursor molecule. Enzymes responsible for ketone body formation are associated mainly with the mitochondria. Steps of synthesis-Acetoacetate (the first ketone body) is formed from acetyl CoA in three steps (figure ) Another way to get into ketosis is by eating less than 20 grams of carbs — or a slice of bread — per day. So people on a ketogenic diet get about 5 percent of their calories from carbohydrates, 15..
The ketogenesis process occurs in the liver particularly during periods of low food intake, carbohydrate-restrictive diets, starvation, or in untreated type 1 diabetes mellitus. Ketone bodies are transported from the liver to the extrahepatic tissues and converted into acetyl-CoA which then enters the citric acid cycle and is utilized for. In this context, peroxisome proliferator-activated receptor α (PPARα) regulates fatty acid oxidation (FAO) and ketogenesis. During fasting, hepatic PPARα-dependent lipid metabolism depends on fatty acid synthase (FAS) and diet-derived lipid metabolites that work as endogenous PPARα ligands (Chakravarthy et al., 200 Ketogenesis Increased availability of free fatty acids, which provide the major substrate for ketone body formation. Low insulin levels and elevated glucagon, catecholamine, growth hormone, and cortisol levels provide a hormonal milieu that inhibits the hepatic metabolism of acetyl-coenzyme A via the citric acid cycle and triglyceride synthesis. Autophagy is a process of self-cannibalization. Cells capture their own cytoplasm and organelles and consume them in lysosomes. The resulting breakdown products are inputs to cellular metabolism, through which they are used to generate energy and to build new proteins and membranes. Autophagy preserves the health of cells and tissues by replacing outdated and damaged cellular components with. Ketogenesis regulation is performed in four levels: 1) Hormone sensitive lipase - lipolysis in the adipose tissue. 2) Carnitine acyltransferase I - entry of fatty acids to the mitochondrial matrix, where β-oxidation is performed. 3) AcCoA from β-oxidation to ketogenesis rather than to the TCA cycle
Regulation of ketogenesis and the renaissance of carnitine palmitoyltransferase. Diabetes Metab Rev 1989; 5:271. Cook GA, Nielsen RC, Hawkins RA, et al. Effect of glucagon on hepatic malonyl coenzyme A concentration and on lipid synthesis Options: View larger image (or click on image) Download as PowerPoint (A) The pathways measured by the simultaneous administration of 5 stable isotope tracers are presented. Ketone tracers allow for the measurement of ketogenesis. The glucose and heavy water tracers allow for the sources of glucose, as well as EGP, to be determined HCO3- is ~ 20 Less buffering capacity Ketogenesis is accelerated 2-4 times during pregnancy Less hyperglycemia is required to cause DKA during pregnancy Mortality: Maternal 5-15% Fetal 50-90% Metabolic Effects of DKA Abnormal Insulin:Glucagon ratio favors triglyceride release from adipose tissue
Ketogenesis & Ketolysis Ketosis ( ketoacidosis ) Metabolism of Cholesterol. Ketogenesis. It is the formation of ketone bodies in the liver mitochondria. Ketone bodies are: CH3-CO-CH2-COOH Acetoacetic acid CH3-CHOH-CH2-COOH β - hydroxybutyric acid Slideshow 3310277 by fisseh In response to undernutrition, short- (days) and medium-term (weeks) adaptations are more pronounced for splanchnic organs than for other tissues. For the latter, the long-term response involves a sequential mobilization (fat > muscle > bone) with relative priorities differing among anatomical agement is to suppress ketogenesis, reduce blood glucose and correct electro-lyte imbalance. Insulin therapy increases peripheral glucose use and decreases hepatic glucose production, thereby low-ering blood glucose concentration. It inhibits the release of free fatty acids from adipose tissues and decreases ketogenesis (Umpierrez et al, 2002) Cholesterol synthesis starts with acetyl-CoA, which is used to synthesize hydroxymethylglutaryl-CoA (HMG-CoA). The reactions in this initial stage are the same as in ketogenesis (see slide 10.4.1).However, while ketogenesis occurs in the mitochondria, HMG-CoA destined for sterol synthesis is formed in the cytosol