Carbs/Lipids as macronutrients
Which organ is primarily responsible for the breakdown of Maltotriose?
Upper Jejunum
What is the rate-limiting enzyme of Fatty acid oxidation?
CPT-1
What is the primary product of de novo fatty acid synthesis, and how many carbons does it contain?
The primary product is palmitate (palmitic acid, C16:0), which contains 16 carbons
What enzyme is the rate-limiting step of de novo cholesterol synthesis?
HMG-CoA reductase, an SER-associated enzyme
Which lipoprotein is responsible for transporting dietary triglycerides to adipose
Chylomicrons
Which of the following best describes the primary underlying cause of Type 1 Diabetes Mellitus?
Autoimmune destruction of pancreatic beta-cells, leading to absolute insulin deficiency.
A 10-month-old infant presents with severe diarrhea, failure to thrive, and protein malabsorption. The underlying cause is determined to be a congenital absence of the critical enzyme found on the luminal surface of intestinal cells responsible for initiating the activation cascade of pancreatic proteases.
Which enzyme is most likely deficient in this patient?
Enteropeptidase
Which vitamin-derived cofactor is required for all aminotransferase reactions?
Pyridoxal phosphate (Vitamin B6)
What is the end product of purine degradation in humans
Uric acid
Purines (adenine, guanine) are broken down into hypoxanthine → xanthine → uric acid via xanthine oxidase. Humans lack uricase (present in many mammals), so uric acid is the final product. Excess uric acid can precipitate in joints, leading to gout.
Why do ketone bodies increase the risk of hyperuricemia?
They compete with urate for excretion in the proximal tubule
This enzyme catalyzes the first committed step in pyrimidine biosynthesis and is positively regulated by PRPP and ATP but inhibited by UTP.
CPS II
A patient presents to the hospital with symptoms of hepatomegaly, fasting hypoglycemia, seizures, and a doll-like face. Name two of the metabolic abnormalties you may find in this patient.
Type 1a Glycogen Storage Disease (von Gierke)
lactic acidemia
hyperuricemia
hyperlipidemia
nephromegaly
Patients following ketogenic or Atkins diets often experience rapid weight loss during the first week, followed by a slower, more gradual decline in weight. What is the primary source of this initial rapid weight loss?
Glycogen is lost first and carries a lot of water weight
Why is diabetic ketoacidosis (DKA) rare in type 2 diabetes compared to type 1?
Type 2 patients have higher baseline insulin levels.
Even in uncontrolled type 2 diabetes, insulin levels are usually sufficient to suppress massive ketogenesis, preventing DKA. In contrast, type 1 diabetes patients lack insulin almost completely
A patient reports to the clinic with gallbladder pain. Later on in the visit, it is discovered that the pain stems from a buildup of bile salts in the gallbladder, and that lipids in the GI tract of the patient have not been getting properly emulsified. What is the likely protein deficiency of this patient resulting in these conditions?
CCK - bile salts are building up in the gallbladder and not being released due to a CCK deficiency preventing bile salt release.
How do elevated levels of glucagon affect lipolysis?
They Don’t. (slide 9) - Lipolysis is stimulated by low insulin and elevated epinephrine.
Why is citrate transported from the mitochondria to the cytosol during the fed state?
Because acetyl-CoA cannot cross the mitochondrial membrane,
it is instead converted into citrate, which can cross into the cytosol. In the cytosol, citrate is cleaved by ATP-citrate lyase to produce acetyl-CoA, the substrate for fatty acid synthesis
Why is cholesterol synthesis more active in the fed state compared to the fasting state?
In the fed state, the insulin/glucagon (I/G) ratio is high. This promotes dephosphorylation and activation of HMG-CoA reductase
Which drug increases serum HDL by decreasing Apo A-I breakdown?
Niacin
In a state of untreated Diabetic Ketoacidosis (DKA), the metabolic profile is characterized by a massive over-reliance on which
Free fatty acids released from adipose tissue.
A 15-year-old patient who is currently undergoing puberty and experiencing a rapid growth spurt is recovering well after a serious bone fracture, a period also referred to as convalescence. This patient is consuming a high-protein diet. The body's nitrogen status for this patient is most likely to be in a state of:
A. Zero nitrogen balance
B. Positive nitrogen balance
C. Negative nitrogen balance
D. Neutral nitrogen balance
E. Negative caloric balance
B. Positive nitrogen balance
Positive nitrogen balance occurs when the amount of nitrogen incorporated (through protein synthesis for growth) exceeds the
amount of nitrogen excreted (as urea or NH^4+. This state is physiologically associated with Growth (puberty/growth spurt) and
Convalescence (recovery from injury/surgery). The body is accumulating net protein mass for tissue repair and formation. Negative nitrogen
balance is associated with catabolic states such as starvation, trauma, or infection.
Which factor allosterically activates carbomoyl phosphate synthetase I (CPSI)
N-acetylglutamate
This molecule, derived from ribose-5-phosphate, is the activated sugar required for nucleotide synthesis.
PRPP
PRPP is derived from ribose-5-phosphate (PPP) and provides the ribose-phosphate backbone for both purine and pyrimidine nucleotides. Without PRPP, nucleotide synthesis cannot begin.
Allopurinol helps prevent gout attacks by .... ?
Inhibiting xanthine oxidase to decrease uric acid production
Unlike purines, pyrimidines are salvaged primarily at this level. Why is that the case?
A. Nucleotides
B. Nucleosides
C. Free bases
D. Ribonucleotides
E. Deoxynucleotides
B. Nucleosides
Explanation: Pyrimidine salvage occurs mostly at the nucleoside level (e.g., uridine → UMP). Free base salvage is inefficient, unlike purines.
What metabolic pathway is accelerated to cause ammonia build up in a patient with carnitine deficiency?
amino acid catabolism
Carbamoyl Phosphate Synthetase 1 (CPS1) is the rate-limiting enzyme in the urea cycle. It has an essential cofactor. What enzyme catalyzes the reaction that makes this coenzyme?
N-acetylglutamate synthetase; it catalyzes the reaction making the cofactor N-acetylglutamate
What is the primary cause of the fruity odor in the breath of a patient with diabetic ketoacidosis (DKA)
Accumulation of acetone
In DKA, acetone—a volatile ketone body—is produced during ketogenesis. It is exhaled and gives the breath a fruity odor
A patient reports to the clinic experiencing intense bloating and flatulence. The patient has been eating a large amount of processed foods lately, with an excessive amount of added sugars. Patient is given an oral sugar tolerance test, and is determined to have a deficiency in the enzyme used in breaking down sucrose.
The physician decides that enzyme replacement therapy is the best treatment for this patient.
What type of bonds must the newly introduced enzyme be able to cleave?
A 1,2 glycosidic bonds
An individual has a blood test and is discovered to have extremely low lipid levels. The patient’s blood test also reflects low Malonyl CoA levels. What is likely the root cause of the patients low blood lipid and Malonyl CoA levels?
Patient has an ACC deficiency (Acetyl CoA Carboxylase)
which results in a lack of production of Malonyl CoA. Malonyl CoA is an allosteric inhibitor of CPT-1 that is active in the Fed state, and prevents FA’s from being immediately oxidized. With no Malonyl CoA, the Carnitine shuttle is fully active and will quickly deplete blood lipid levels.
How is acetyl-CoA carboxylase (ACC), the rate-limiting enzyme of fatty acid synthesis, regulated allosterically?
Activated by: citrate (feed-forward activation, promotes polymerization of ACC)
Inhibited by: long-chain fatty acyl-CoA, especially palmitoyl-CoA (feedback inhibition, prevents excessive synthesis
How does cytosolic cholesterol regulate its own intracellular homeostasis? ( 3 things)
High cytosolic cholesterol levels:
Decrease HMG-CoA reductase expression (less new cholesterol made).
Decrease LDL receptor expression (less cholesterol imported from blood).
Activate ACAT, promoting storage as cholesterol esters
A patient presents with eruptive xanthomas and pancreatitis after a fatty meal. Labs show markedly elevated triglycerides and turbid serum. Which defect is most likely?
Apo C-II deficiency
A 12-year-old girl with newly diagnosed Type 1 Diabetes Mellitus (T1DM) is admitted to the emergency department with altered mental status, Kussmaul respirations, and a fruity odor on her breath. Laboratory findings show plasma glucose of 450 mg/dL, arterial pH of 7.05, and 4+ urinary ketones.
The patient's condition is directly caused by an extremely low insulin-to-glucagon (I/G) ratio, which triggers a cascade of catabolic metabolic events.
Which of the following is the most direct biochemical consequence of the low I/G ratio that leads to the massive overproduction of ketone bodies?
A. Increased glucose uptake by muscle and adipose tissue via GLUT-4.
B. Increased synthesis of Malonyl-CoA, which inhibits fatty acid beta-oxidation.
C. Activation of Hormone-Sensitive Lipase (HSL) leading to a massive flux of free fatty acids to the liver.
C. Activation of Hormone-Sensitive Lipase (HSL) leading to a massive flux of free fatty acids to the liver.
An extremely low insulin/glucagon ratio, combined with elevated counter-regulatory hormones like epinephrine, causes the activation of
Hormone-Sensitive Lipase (HSL) in adipose tissue. This results in excessive lipolysis, flooding the bloodstream and the liver with free fatty acids. In the liver, the
high flux of fatty acids, combined with the low I/G ratio suppressing Malonyl-CoA (an inhibitor of the carnitine shuttle), leads to very active beta-oxidation and
subsequent massive ketogenesis.
A 45-year-old man presents to the emergency room in a state of starvation after being lost in the wilderness for three weeks. His blood glucose is low, and his body is attempting to maintain normal glucose homeostasis by relying heavily on endogenous sources.
In this scenario, which of the following statements most accurately describes the metabolic fate of the majority of amino acid carbon skeletons being mobilized for energy and glucose production?
A. They are converted into TCA cycle intermediates (without consuming OAA) and then into glucose.
B. They are primarily converted into acetyl-CoA for direct use in gluconeogenesis.
C. They are first deaminated, and the resulting carbon skeletons are used directly as fuel for muscle contraction.
A. They are converted into TCA cycle intermediates (without consuming OAA) and then into glucose.
They are converted into TCA cycle intermediates (without consuming OAA) and then into glucose.
Explanation: In prolonged starvation, the body relies on glucogenic amino acids (most amino acids) to maintain blood glucose levels. The carbon skeletons
of these amino acids are converted into TCA cycle intermediates (such as succinyl CoA, fumarate, alpha-ketoglutarate, oxaloacetate), which leads to a net
increase in oxaloacetate (OAA). OAA is the key precursor that enters the gluconeogenesis pathway to be converted into glucose. Ketogenic amino acids
(leucine and lysine) form acetyl-CoA or acetoacetate, which cannot be used for net glucose synthesis.
In periportal hepatocytes, glutamate serves as a key nitrogen donor. A patient with impaired nitrogen handling but normal transaminases demonstrates abnormal urea production.
Which two pathways allow glutamate to provide nitrogen for incorporation into urea?
A. Aspartate + CPSI
B. Aspartate and free NH3
C. Alanine and NH3
D. Glutamine and NH4+
B. Aspartate and free NH3
Glutamate donates nitrogen via (1) deamination (free NH₃) and (2) transamination to aspartate.
In de novo purine synthesis, the cell uses this nucleotide as an energy source to make AMP, while the reciprocal nucleotide powers GMP formation.
GTP for AMP, ATP for GMP
AMP synthesis requires GTP, and GMP synthesis requires ATP. This reciprocal use prevents overproduction of one nucleotide and helps maintain AMP:GMP balance.
Increased urate production leading to hyperuricemia can be due to all of the following EXCEPT
A. Decreased efficiency of purine salvage
B. Overactive PRPP synthetase
C. Increased rate of purine degradation
D. Increased renal clearance of urate
D. Increased renal clearance of urate
Increased renal clearance of urate lowers uric acid levels, leading to hypouricemia, not hyperuricemia.
This enzyme catalyzes the rate-limiting step of DNA synthesis by converting dUMP into dTMP using N5,N10-methylene-THF as a cofactor.
Thymidylate synthase
Thymidylate synthase converts dUMP → dTMP. Critical for DNA synthesis, requires N5,N10-methylene-THF. Without it, DNA replication halts.
What monosaccharides (2) should be limited in patients with von Gierke disease?
fructose and galactose
How does hyperammonemia lead to increased excitotoxicity and cell death in the neurons?
Increased blood ammonia —-> increased ammonium (NH4+) in the brain —> increased glutamate production. Glutamate is an excitatory neurotransmitter and too much of it can lead to cell death
What is the primary cause of fruity odor in the breath of a patient with diabetic ketoacidosis (DKA)
Accumulation of acetone
A patient frequently complains of bloating and gas after eating cooled starchy foods like cold rice or potatoes. Breath testing shows increased hydrogen levels. Which of the following best explains the biochemical mechanism and clinical outcome?
a) Retrograde starch is more bioavailable, leading to rapid glucose absorption and hyperglycemia.
b) Retrograde starch resists digestion, is fermented by colonic bacteria, and increases gas formation.
c) Retrograde starch enhances amylase activity, producing excess maltose and osmotic diarrhea.
d) Retrograde starch directly inhibits GLUT-2 transporters, reducing monosaccharide absorption.
b) Retrograde starch resists digestion, is fermented by colonic bacteria, and increases gas formation
Explanation: Cooling of starch leads to retrogradation, where amylose chains re-crystallize and expel water, making the starch less digestible. Because α-amylase has limited access, undigested starch reaches the colon and is fermented by bacteria, producing gases (CO₂, H₂, methane), explaining the bloating and breath test results.
A medical student fasts for 24 hours. During this time, β-oxidation is very active, generating large amounts of NADH and ATP. Which of the following BEST explains why most acetyl-CoA from β-oxidation is shunted into ketogenesis instead of the TCA cycle?
a) High NADH levels inhibit isocitrate dehydrogenase, slowing the TCA cycle.
b) ATP directly activates HMG-CoA synthase, forcing acetyl-CoA into ketogenesis.
c) The carnitine shuttle is inhibited, preventing acetyl-CoA entry into the mitochondria.
d) Malonyl-CoA accumulates, preventing TCA cycle entry of acetyl-CoA.
a) High NADH levels inhibit isocitrate dehydrogenase, slowing the TCA cycle
Explanation: During fasting, β-oxidation produces high levels of NADH and ATP. These molecules inhibit isocitrate dehydrogenase, the rate-limiting enzyme of the TCA cycle. As a result, acetyl-CoA accumulates and is diverted to ketogenesis, producing ketone bodies as an alternative fuel for the brain and muscle.
Explain why malonyl-CoA plays a dual role in lipid metabolism and how this prevents a futile cycle.
Malonyl-CoA is both:
The building block for fatty acid synthesis (2-carbon donor).
An inhibitor of carnitine palmitoyltransferase I (CPT I), preventing fatty acid β-oxidation
Explain how bile acid sequestrant drugs (like cholestyramine) lower serum LDL cholesterol.
They bind bile acids in the intestine, preventing reabsorption.
Since more bile acids are lost, the liver must synthesize new ones using cholesterol.
This lowers cytosolic cholesterol, upregulates LDL receptors, and increases LDL uptake from blood
A nascent HDL particle acquires cholesterol from a peripheral cell via ABCA1. Which step ensures that the cholesterol remains trapped inside the HDL particle
LCAT esterification of cholesterol
A 45-year-old man with a BMI of 35 kg/m^2 has been managing a state of compensated insulin resistance (IR/Pre-diabetes, Phase I) for five years, characterized by hyperinsulinemia maintaining near-normal blood glucose. However, recent lab work shows a fasting glucose of 150 mg/dL (overt diabetes) and a corresponding plasma insulin level that has decreased from its previous peak.
This patient's transition from a compensated, insulin-resistant state to overt Type 2 Diabetes Mellitus (Phase II) is primarily due to the failure of which compensatory mechanism?
A. Development of severe Hyperosmolar Syndrome.
B. Increased tissue uptake of glucose, leading to beta-cell exhaustion.
C. Inability of pancreatic beta-cells to sustain the high rate of insulin production, leading to beta-cell dysfunction/exhaustion.
C. Inability of pancreatic beta-cells to sustain the high rate of insulin production, leading to beta-cell dysfunction/exhaustion.
The progression from insulin resistance (Phase I) to overt Type 2 Diabetes Mellitus (Phase II) is defined by the failure of the pancreatic beta-cells to continue compensating for the IR by producing excessive insulin. When the beta-cells become exhausted and their insulin secretion falls (even if it's still "above normal" for a short period), the blood glucose level can no longer be controlled, and overt diabetes is diagnosed. Insulin resistance alone is insufficient to cause the disease.
A patient with chronic liver failure develops a state of hepatic encephalopathy, exhibiting confusion and altered mental status due to elevated plasma levels of ammonia and other toxins. The dietary management of this condition often involves the restriction of total protein intake.
However, specialized nutritional supplements are sometimes used to provide amino acids that may have a therapeutic effect. Which class of amino acids is often supplemented in these patients to potentially reduce ammonia production and compete with tryptophan uptake into the brain?
A. Branched-Chain Amino Acids (BCAAs): Leucine, Isoleucine, and Valine
B. Essential aromatic amino acids: Phenylalanine, Tyrosine, and Tryptophan
C. Glucogenic amino acids: Alanine and Glutamine
A. Branched-Chain Amino Acids (BCAAs): Leucine, Isoleucine, and Valine
Explanation: BCAAs (Leucine, Isoleucine, Valine) are often used in the nutritional support of patients with hepatic encephalopathy. They are preferentially
metabolized in muscle rather than the liver, thus reducing the hepatic nitrogen load. Furthermore, they share the same transporter across the blood-brain
barrier as aromatic amino acids (like Tryptophan), effectively competing for uptake. Reducing the uptake of Tryptophan is important as it is a precursor for
the false neurotransmitter serotonin, which is thought to contribute to the neurological symptoms.
A 3-day-old newborn presents with poor feeding, vomiting, lethargy, and an unusual sweet odor to the urine. Parents report increasing irritability and drowsiness. On metabolic screening, plasma amino acid analysis shows markedly elevated branched-chain amino acids. Which metabolite is most diagnostic for this disorder?
A. Citrulline
B. Aspartate
C. L-alloisoleucine
D. Fumarate
C. L-alloisoleucine
Elevated L-alloisoleucine is pathognomonic for MSUD.
Maple syrup urine disease is caused by decreased activity of the branched-
chain α-ketoacid dehydrogenasecomplex (BCKD)
Both BCAAs (Ile, Leu, Val) and their α- ketoacids accumulate in the
bloodstream
A deficiency of this vitamin impairs purine synthesis, disrupting DNA replication and causing megaloblastic anemia due to delayed nuclear maturation in RBCs.
Folate (Vitamin B9)
Folate is needed to form tetrahydrofolate (THF), which donates one-carbon units in purine synthesis. Folate deficiency halts DNA synthesis, leading to megaloblastic anemia where nuclear maturation is impaired.
In patients with gout, hyperuricemia leads to deposition of monosodium urate crystals on articular cartilage. Which event directly causes joint damage?
A. Sodium and urate diffusing into interstitial fluid
B. Phagocytosis of urate crystals by neutrophils and macrophages
C. Release of lysosomal and cytosolic enzymes after cell lysis
D. Formation of tophi from uric acid crystals
C. Release of lysosomal and cytosolic enzymes after cell lysis
Explanation: urate crystals inside neutrophils cause lysosomal rupture → neutrophil death → uncontrolled release of proteases, reactive oxygen species, and inflammatory mediators into the synovial fluid. These enzymes and ROS digest articular cartilage and damage synovial tissue. This is the immediate mechanism that injures the joint.
Accumulation of this deoxynucleotide inhibits ribonucleotide reductase and leads to Severe Combined Immunodeficiency (SCID).
dATP
ADA deficiency → buildup of deoxyadenosine → converted to dATP. Excess dATP inhibits ribonucleotide reductase, preventing production of other dNTPs → defective DNA synthesis → SCID.
What enzyme promotes increased glucose clearance from blood through the translocation of GLUT4 to the surface of muscle cells in carnitine deficient individuals?
AMPK
A 9-month-old infant with OTC deficiency presents with hyperammonemia and elevated urinary orotic acid. Which of the following BEST explains why orotic acid accumulates in this condition?
a) Carbamoyl phosphate leaks from mitochondria into the cytoplasm, driving pyrimidine synthesis beyond PRPP availability.
b) Excess nitrogen from glutamine breakdown directly activates pyrimidine biosynthesis.
c) Ammonia inhibits CPSII, trapping intermediates in the orotic acid pathway.
d) UTP accumulation directly stimulates orotic acid synthesis.
a) Carbamoyl phosphate leaks from mitochondria into the cytoplasm, driving pyrimidine synthesis beyond PRPP availability
In OTC deficiency, carbamoyl phosphate builds up in mitochondria and spills into the cytoplasm, where it fuels pyrimidine biosynthesis independent of CPSII regulation. The resulting overproduction of intermediates, combined with decreased clearance due to low PRPP, causes orotic aciduria, a diagnostic hallmark of OTC deficiency.
A patient with type 2 diabetes is prescribed metformin. Which of the following best explains how it reduces fasting blood glucose?
a) It increases hepatic gluconeogenesis and lowers insulin sensitivity.
b) It activates AMPK, which decreases gluconeogenesis and increases GLUT-4 translocation.
c) It inhibits GLUT-4 transporters in muscle, preventing hyperglycemia.
d) It directly blocks pancreatic β-cell apoptosis.
b) It activates AMPK, which decreases gluconeogenesis and increases GLUT-4 translocation.
Metformin activates AMPK, shifting metabolism toward glucose uptake in muscles and reducing hepatic glucose production, lowering fasting blood glucose
A child in Jamaica consumes unripe ackee fruit and develops profound hypoglycemia, vomiting, and coma. Which of the following BEST explains why hypoglycemia occurs in this condition?
a) Hypoglycin A inhibits glycogen phosphorylase, preventing glycogen breakdown.
b) Inhibition of β-oxidation reduces ATP production, impairing gluconeogenesis.
c) The TCA cycle becomes hyperactive, consuming too much glucose.
d) Ketogenesis is increased, preventing glucose availability for the brain.
b) Inhibition of β-oxidation reduces ATP production, impairing gluconeogenesis
Unripe ackee fruit contains hypoglycin A, which is metabolized into compounds that inhibit β-oxidation enzymes. Without β-oxidation, ATP and NADH production falls dramatically. Since gluconeogenesis requires ATP (for pyruvate carboxylase and other steps), it fails, leading to profound hypoglycemia despite ongoing lipolysis. This explains the severe clinical presentation of Jamaican vomiting sickness.
A patient is given a drug that chronically activates AMPK. Predict how this would affect lipogenesis and explain why.
Lipogenesis would be inhibited.
AMPK phosphorylates and inactivates ACC, decreasing malonyl-CoA production.
With less malonyl-CoA, fatty acid synthesis is reduced, and β-oxidation is favored
A patient has a mutation in the LDL receptor gene (familial hypercholesterolemia). Predict the effects on cholesterol metabolism and serum lipid profile.
Impaired LDL receptor activity → less LDL endocytosis.
Serum LDL cholesterol rises dramatically (very high LDL, but normal TAGs).
Cytosolic cholesterol remains low, so HMG-CoA reductase activity and de novo synthesis increase
A 45 year old man presents with premature coronary artery disease. His labs show very low HDL and LDL, but elevated fasting nascent CM and VLDL. His tonsils appear large and orange. Which underlying protein deficiency explains these findings?
ABCA1
A 7-year-old girl with a urea cycle disorder presents with confusion and irritability after a high-protein meal. MRI shows diffuse brain edema. Which molecular mechanism explains the cerebral swelling in hyperammonemia?
NH₄⁺ combines with glutamate to form glutamine, which is osmotically active.
Ammonia detoxified in astrocytes via glutamine synthetase; glutamine buildup draws water, causing edema.
This chemotherapeutic agent blocks dihydrofolate reductase (DHFR), preventing regeneration of THF and thereby halting purine synthesis in rapidly dividing cells.
A. 5-Fluorouracil
B. Azathioprine
C. Hydroxyurea
D. Methotrexate
D. Methotrexate
Methotrexate inhibits DHFR, blocking regeneration of THF. Without THF, purine (and thymidylate) synthesis stops, which especially impacts rapidly dividing cells like cancer cells. Side effects include bone marrow suppression and mucositis.
This drug is a suicide inhibitor of thymidylate synthase, effective only when converted into its nucleotide form (F-dUMP), and is used in cancer therapy.
5-Fluorouracil
5-FU is converted to F-dUMP, which irreversibly binds thymidylate synthase, blocking dTMP synthesis. Used in cancer therapy (systemic and topical).
A patient has been on a ketogenic diet for several weeks. Compare their metabolism to someone who has been fasting for 48 hours. Which of the following BEST describes a key difference between the two states?
a) The ketogenic dieter depends mainly on muscle proteolysis for gluconeogenic precursors, whereas the fasting patient relies on dietary amino acids.
b) The ketogenic dieter still has slight insulin release from dietary protein, limiting muscle breakdown, whereas the fasting patient has lower insulin and greater muscle catabolism.
c) The ketogenic dieter produces ketone bodies at a much higher rate than the fasting patient because of unrestricted fat intake.
d) The fasting patient maintains higher glycogen stores compared to the ketogenic dieter.
b) The ketogenic dieter still has slight insulin release from dietary protein, limiting muscle breakdown, whereas the fasting patient has lower insulin and greater muscle catabolism
Both ketosis and fasting promote gluconeogenesis and ketogenesis. However, in a ketogenic diet, dietary protein stimulates some insulin secretion, sparing muscle from excessive breakdown. In prolonged fasting, insulin is very low, muscle catabolism accelerates, and amino acids become the main gluconeogenic substrate. This subtle but important distinction explains why muscle wasting is less severe on high-protein, low-carb diets compared to starvation.
A patient with obesity and type 2 diabetes is switched from sulfonylureas to GLP-1 mimetic therapy. Which of the following is the most likely clinical benefit of this change?
a) Increased risk of hypoglycemia
b) Further weight gain due to higher insulin secretion
c) Appetite suppression and delayed gastric emptying
d) Elimination of the need for lifestyle changes
c) Appetite suppression and delayed gastric emptying
GLP-1 mimetics enhance insulin secretion only when glucose is present, while also inhibiting appetite and delaying gastric emptying. This helps reduce postprandial hyperglycemia and supports weight loss