Protein
List 6 major functions of proteins in the body.
What are
1. Enzymes (e.g., lipase)
2. Storage (e.g., ferritin)
3. Transport (e.g., hemoglobin)
4. Contractile (e.g., myosin)
5. Immune (e.g., antibodies)
6. Hormones (e.g., insulin) / Structural (e.g., collagen)?
Major difference between GIP and GLP-1?
GLP-1 → reduces intake via increased satiety, reduced appetite, increased insulin, reduced gastric emptying
GIP → modulates storage by increasing insulin
Components of the 4-component body composition model?
What are
Fat mass, total body water, bone mineral content, protein mass?
"Wearable" definition
What is
Body-worn or implanted device
Continuously measures physiological signals
Provides real-time or near real-time data?
An athlete stops exercising for a month and loses endurance. What happened to her muscle fibers?
What is Type IIa fibers convert to IIx (more glycolytic), reducing oxidative capacity?
Two conditionally essential amino acids that become indispensable during critical illness, trauma, or metabolic stress due to increased demand and inadequate endogenous synthesis.
What are glutamine and arginine? (Accept also: cysteine, tyrosine, or citrulline)
When are AOMs clinically indicated?
What are
BMI ≥30 kg/m², or BMI ≥27 kg/m² with weight-related comorbidity
Continue only if clinically meaningful response occurs (≥5% weight loss at ~12 weeks on therapeutic dose)?
The definition of Energy Availability (EA) and the threshold for physiological dysfunction.
What is EI - EEE / kg FFM/day — with dysfunction at <30 kcal/kg FFM/day?
3 Wearable devices
What is
Non-invasive (wrist, patch, chest strap)
Minimally invasive (e.g., CGM)
Implanted (pacemakers, defibrillators)?
A 68-year-old patient on tirzepatide has lost 15% body weight but 35% of that loss is lean mass by DEXA. Using the concept of anabolic resistance, explain why this patient lost more lean mass than expected and prescribe the specific protein intervention.
What is anabolic resistance of aging blunts MPS response to amino acids — requiring higher per-meal protein: 0.4 g/kg/meal, 2–3 g leucine/meal, total 1.2–1.6 g/kg/day?
The specific leucine threshold (grams per meal) required to maximally stimulate muscle protein synthesis, and why older adults with anabolic resistance may need more.
What is ~2–3 g leucine/meal, with older adults potentially needing higher doses due to blunted mTOR signaling?
List the 4 GLP-1 RA types
What are
Exenatide = early analog (DPP-4 resistant, shorter-acting)
Semaglutide = long-acting GLP-1 analog (enhanced stability, weekly dosing)
Tirzepatide = dual agonist (GLP-1 + GIP)
Retatrutide = triple agonist (GLP-1 + GIP + glucagon)?
Describe the active transport mechanism for getting amino acids into an enterocyte.
Sodium (Na+) enters the cell along with the amino acid. The sodium is then exchanged for potassium (K+) via the Na/K pump.
Two specific biological fluids that emerging wearable devices can analyze (from the multi-site diagram).
What are saliva, sweat, tears, breath, urine, interstitial fluid (ISF) via microneedle, wound fluid, or stool? (Any two)
A patient with phenylketonuria (PKU) follows an amino acid-restricted diet low in phenylalanine but consumes medical foods to supply remaining EAAs. Using the concept of nitrogen balance, explain why simply restricting phenylalanine without EAA supplementation leads to negative nitrogen balance and muscle wasting.
What is phenylalanine restriction alone creates deficiency of an EAA → protein synthesis cannot proceed → MPS < MPB → negative nitrogen balance. Medical foods provide all other EAAs in correct proportions, allowing positive nitrogen balance despite phenylalanine restriction?
The specific daily protein turnover in grams (synthesis and degradation), typical protein lifespan in days, and how much nitrogen is lost daily.
What are 200–300g synthesized/degraded daily, <2 days typical lifespan, and ~60g nitrogen lost/day?
The absolute contraindications for AOMs?
What are
Personal or family history of medullary thyroid carcinoma (MTC) or MEN2
Pregnancy / planned pregnancy ?
What are 7 examples of protein-modified diets?
What are
1. High-Protein – Sarcopenia, post-surgical recovery, trauma, weight loss, athletes
2. Low-Protein – CKD, renal insufficiency
3. Protein-Sparing Modified Fast – Pre-bariatric surgery, severe obesity
4. Amino Acid-Restricting – PKU, MSUD, homocystinuria
5. Plant-Based – CVD, T2DM, CKD, ethical/religious dietary pattern
6. High-Protein:Low-CHO – epilepsy, IR, metabolic syndrome
7. Protein Supplement-Augmented – cancer, elderly, post-operative, athletes
unable to meet protein needs, malnutrition?
The difference between targeted and untargeted metabolomics in terms of approach, sensitivity, and clinical applicability.
What is targeted = predefined metabolites, high sensitivity, pathway-specific, clinically actionable — untargeted = broad coverage, biomarker discovery, captures global metabolic state, complex interpretation?
Two patients eat the same meal. Patient A (young, lean, active) oxidizes most of the meal energy. Patient B (older, obese, sedentary) stores more as fat. Name the three interconnected concepts that explain this difference.
What are (1) insulin resistance, (2) low metabolic rate from low muscle mass, (3) low NEAT/activity energy expenditure (or set point dysregulation, reduced fat oxidation capacity, impaired glucose disposal)?
The three clinical applications of a Protein-Sparing Modified Fast (PSMF) and its macronutrient composition.
What are (1) pre-bariatric surgery, (2) severe obesity, (3) rapid weight loss with lean mass preservation — with very low calorie, high protein, minimal CHO and fat?
The percentage of AOM-induced weight loss that may be lean mass (from NEJM), and the two interventions to prevent it.
What is 20–40% lean mass loss — prevented by adequate protein intake (1.2–1.6 g/kg/day) and resistance training?
The difference between energy balance (passive) and energy homeostasis (regulated) — and why obesity is considered a dysregulation of the latter.
What is energy balance = calories in vs out (mathematical); energy homeostasis = regulated biological system (brain-gut-adipose signaling) — obesity = impaired signaling (e.g., leptin resistance)?
The major current hurdle for wearable integration into nutrition practice (shown as a figure in Lecture 16) and why it matters clinically.
What is weak multi-sensor integration — because individual data streams (HR, glucose, temperature, movement) are not yet synthesized into actionable, individualized nutrition recommendations?
This concept from Lecture 17, emphasized with "(this is a key point to understand) (wink, wink → Exam 3)," explains why dieting alone triggers increased hunger (ghrelin ↑, leptin ↓) and decreased energy expenditure (adaptive thermogenesis), while AOMs restore regulatory control by overriding this biologically defended value.
What is the set point (or biologically defended energy balance set point)?