Controlling Metabolism
Energy Balance and Exposure
Anabolic vs. Catabolic
Diabetes
Fructose
100

NPY acts on what integration center?

Feeding Center (lateral hypothalamus)

100

Input <, >, or = for the following:

Male BMR _ Female BMR

Young BMR _ Old BMR

Endurance trained BMR _ Non-trained BMR

Male BMR > Female BMR

Young BMR > Old BMR

Endurance trained BMR < Non-trained BMR

100

What is anabolic? What is catabolic?

Anabolic = eating

Catabolic = not eating/fasting

100

What is the difference between Type I diabetes and Type II diabetes?

Type I: Beta cells (secrete insulin, amylin) destroyed by autoimmune response; born with it

Type II: Insulin receptors no longer responsive to insulin; develop it

100

What is sucrose?

Glucose + fructose

200

How are glucostatic and lipostatic theory connected?

Neuropeptide Y (NPY)  has preference for carbohydrate intake (glucose!), leptin (exocrine) is released from adipose tissue → stops hunger by shutting down NPY in hypothalamus

200

Direct calorimetry is determined by ____ produced.

Indirect calorimetry is determined by __ consumption and ___ production. 

Direct calorimetry is determined by heat produced.

Indirect calorimetry is determined by O2 consumption and CO2 production.

200

Liver cells have what kind of glucose of GLUT transporter? How does it work?

BONUS (x2): Are these receptors bringing glucose in or out when low and high plasma [glucose]?

GLUT 2 transporters are channels that are always there for glucose (not regulated like GLUT 4 with insulin).

BONUS (x2) Bringing glucose out when plasma [glucose] is low because glycogen stores are being broken down inside the cell. Pulling glucose in when plasma [glucose] is high to increase glycogen stores. 

200

Name at least 3 diabetes illnesses. 

  • heart & blood vessel disease

  • nerve damage

  • kidney damage

  • eye damage

  • foot damage

  • skin & mouth conditions

  • pregnancy complications

200

In hepatocyte glucose metabolism, SRBP1 upregulates transcription factors for what enzyme that converts glucose to G6P?

Glucokinase

300
Label the following peptides as "U" (upregulating) or "D" (downregulating) NPY: Ghrelin, Orexins, CCK, Obestatin, Insulin.


BONUS (x2): What are the sources of these peptides?

Ghrelin (U) --> Stomach, Orexins (U) --> Hypothalamus, CCK (D) --> Duodenum, Obestatin (D) --> Stomach, Insulin (D) --> Pancreas.

300

If someone's respiratory quotient is 0.7, are they consuming more fats or glucose? Why?

*hint: RQ=CO2 produced/O2 consumed

More fats

Oxidation of fats results in more O2 consumed than CO2 produced

Glucose CO2 production = O2 consumption

16 CO2 produced / 23 O2 consumed = 0.7 RQ

300

Rank the following for the insulin pathway:

IRS is phosphorylated, Insulin binds to TKA,  Second messenger pathways upregulate GLUT4 production, Glucose enters cell, Glycogen is formed, High plasma [glucose] causes beta cells to secrete insulin, Glucose is tranformed into G6P

High plasma [glucose] causes beta cells to secrete insulin, Insulin binds to TKA, IRS is phosphorylated, Second messenger pathways upregulate GLUT4 production, Glucose enters cell, Glucose is transformed into G6P, Glycogen is formed

300

Reyna is trying to lessen her chances of ever becoming diabetic. Name 3 ways that she can do that. (diet/lifestyle/etc.)

Eat complex sugars (avoid simple ones), Excercise, Avoid high caloric meals, Avoid sedentary lifestyle, Decrease constant eating (fasting sometimes), Eat more proteins/fats than carbs

300

Name 3 negative effects of EtOH digestion in hepatocytes. 

Overloading of calories sent to liver (96 vs. 24), ROS (reactive oxygen species) produced, Dyslipidemia (high cholesterol), Muscle prefers fats over glucose (muscle cells get insulin resistance), VLDL being produced in high amounts, Inflammation of liver (immune system tries to attack)

400

Match the centers with their function in GIT:

1) Cortex-brain 2) Limbic system 3) Lateral-hypothalamus 4) Hormones 5) Ventromedial hypothalamus

A) Feeding Center B) Satiety Center C) to think about food D) eating your emotions E) regulation

1) Cortex-brain --> C) to think about food

2) Limbic system --> D) eating your emotions

3) Lateral-hypothalamus --> A) Feeding Center

4) Hormones --> E) regulation

5) Ventromedial hypothalamus -->B) Satiety Center

400

In the case of excess glucose, determine each statement as T/F.

Glycogenesis occurs. Lipogenesis occurs. Gluconeogenesis occurs. Glucose is excreted through urine. Glycogenolysis occurs.

Glycogenesis occurs. --> T

Lipogenesis occurs. --> T

Gluconeogenesis occurs. --> F

Glucose is excreted through urine. --> T

Glycogenolysis occurs.--> F

400

Amanda is pre-diabetic and is working on getting better by doing intermittent fasting to help her insulin insensitivity and to lose weight.

If you agree with Amanda's method, explain why. If you disagree, explain why and propose a new method.

Amanda is correct. By not eating for periods of time, Amanda's body is secreting glucagon instead of insulin, allowing for her insulin receptors to "rest". Glucagon also up-regulates the liver cells to use fatty acids from adipose stores to make ketones as alternative energy, helping Amanda to lose weight and give her insulin receptors a break.

400

A new drug is proposed to change the GLUT1 receptors on endothelial cells to GLUT4. Would this drug help insulin-resistant people to manage high glucose levels? Why or why not?

The new drug would not help. If GLUT4 was put on the membrane instead of GLUT1, then glucose could not even enter endothelial cells, as insulin resistance inhibits GLUT 4 production. It would stay more trapped in the blood, causing a large cascade of negative effects.

400

Fill in the blank numbers:

120 Cal Glucose --> __ to liver --> __ to blood

120 Cal EtOH --> __ to liver --> __ to blood

120 Cal Sucrose --> 60 fructose, 12 glucose to liver --> 48 glucose to blood

Fill in the blank numbers:

120 Cal Glucose --> 24 to liver --> 96 to blood

120 Cal EtOH --> 96 to liver --> 24 to blood

120 Cal Sucrose --> 60 fructose, 12 glucose to liver --> 48 glucose to blood

500

Fill in the blank:

Stomach emptiness is sensed by the _____ (intrinsic/extrinsic) CNS pathway. ___ (low/high) pH in the stomach senses this and sends signals to the interneurons and then the ____ neurons in the spinal cord. These neurons tell digestive muscles to _____ and secretory cells to _____. Sight/smell of food sensed by the ______ (intrinsic/extrinsic) CNS pathway. These systems are mostly the same, but the extrinsic CNS pathway sends signals to the ______ instead of the spinal cord.  

Stomach emptiness is sensed by the intrinsic CNS pathway. High pH in the stomach senses this and send signals to the interneurons and then the plexus neurons in the spinal cord. These neurons tell digestive muscles to contract and secretory cells to secrete. Sight/smell of food sensed by the Sight/smell of food sensed by the extrinsic CNS pathway. These systems are mostly the same, but the extrinsic CNS pathway sends signals to the brain instead of the spinal cord.

500

Carl wants to body build by doing strength training and only eating lots of fats. He says that fats are good because they contain more energy than carbohydrates, and low glucose levels induce ketosis which is good for turning his own fat storages into muscle. 

If you agree with Carl's method, explain why. If you disagree, explain why and propose a new method.

Carl's method is wrong. Although fats contain more energy than carbohydrates, they are not the best source of energy for bodybuilding. Eating no glucose at all causes gluconeogenesis to occur from the amino acid pool, which degrades the muscle cells. This is the opposite effect of Carl's goal of bigger muscles. Carl should eat lots of protein and a little bit of glucose so that there are lots of amino acids available to build more proteins in his muscles. 

**Carl is partially right in that fats can undergo ketogenesis to give energy to muscle cells, but helping muscle cells grow needs protein.

500

Fill in the blank:

___(low/high) plasma [glucose] causes pancreatic ____ (a cells/b cells) to secrete insulin. Insulin _____ (upregulates/downregulates) glucose transport, glycolysis, and lipid/protein synthesis. Liver cells up-regulate ____ (glyco/gluco)neogenesis. GIP and GLP-1 ______ (upregulate/downregulate) insulin production.

High plasma [glucose] causes pancreatic B-cells to secrete insulin. Insulin up-regulates glucose transport, glycolysis, and lipid/protein synthesis. Liver cells up-regulate glyconeogenesis. GIP and GLP-1 upregulate insulin production.

500

Fill in the blanks for type one diabetes cascade:

  • ____ [Glucose] in plasma

    • Decreased uptake of insulin-sensitive GLUT-4

  • ______ glucagon production

    • Cells “starving” so secretes glucagon

    • Causes cells to break down _____ and make more glucose

  • ______ Ketones

    • ______ are being broken down to make ketones

  • ______ pH

    • Increased ketones ______ pH


  • Increased [Glucose] in plasma

    • Decreased uptake of insulin-sensitive GLUT-4

  • Increased glucagon production

    • Cells “starving” so secretes glucagon

    • Causes cells to break down glycogen and make more glucose

  • Increased Ketones

    • Fatty acids are being broken down to make ketones

  • Decreased pH

    • Increased ketones decrease pH

500

Fill in the blanks (i'm sorry):

1. fructose gets phosphorylated by ATP/fructokinase > forms ADP as "waste"

2. cell gets rid of ADP by AMP deaminase > forms _____ acid > toxic to cell > is removed from cell > "KNOCKS OUT" ______ (vasodilator) > results in vasoconstriction & _______ (increased/decreased) BP

3. F1P converted to either: G3P (increases _____ --> fatty acid synthesis), or F-1,6-BP (converted to ______, which upregulates glycolysis --> fatty acid synthesis)

4. _______ tissue build up causes dyslipidemia and insulin resistance, inflammation.

5. Hyperinsulinemia occurs, confusing the mind. NPY ____ (stays on/turns off), causing you to eat MORE FRUCTOSE (no shut off system)

1. fructose gets phosphorylated by ATP/fructokinase > forms ADP as "waste"

2. cell gets rid of ADP by AMP deaminase > forms uric acid > toxic to cell > is removed from cell > "KNOCKS OUT" nitric oxide (vasodilator) > results in vasoconstriction & ↑ BP

3. F1P converted to either: G3P (increases citrate --> fatty acid synthesis), or F-1,6-BP (converted to xylulose-5-P, which upregulates glycolysis --> fatty acid synthesis)

4. Adipose tissue build up causes dyslipidemia and insulin resistance, inflammation

5. Hyperinsulinemia occurs, confusing the mind. NPY stays on, causing you to eat MORE FRUCTOSE (no shut off system)