5A and 5B- Fuel Metabolism and Carbs Flashcards

1
Q

What is metabolic homeostasis?

A

control of balance between substrate need and substrate availability. This is achieved by: 1) level of fuel or nutrients in the blood affects the rate at which they are used or stored in different tissues. 2) level of one of the hormones of metabolic homeostasis. 3) Nerve impulses (CNS) that affect tissue metabolism or the release of hormones

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2
Q

Where does insulin come from?

A

Insulin is released from β-cells (these cells must be bathed in glucose) in the pancreas (Islets of Langerhans)

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3
Q

When is [insulin] highest and lowest in the blood?

A

Insulin is in highest concentration 30-45 mins after a meal and lowest 120 mins after a meal

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4
Q

What are the functional roles of insulin?

A

major anabolic hormone of the body that promotes storage of nutrients: glucose –> glycogen (liver and muscles), Glucose –> TG’s (in liver) and their storage in adipose tissue, and lastly aa uptake and protein synthesis in skeletal muscle. Insulin also promotes the utilization of glucose as a fuel by aiding its transport into the muscle and adipose tissue. Insulin inhibits fuel mobilization (ex: gluconeogenesis)

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5
Q

What 2 things in the liver does glucagon do?

A

Gycogenolysis, gluconeogenesis of lactate, AA’s and glycerol

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6
Q

What does glucagon do in the adipose tissue?

A

mobilize FA’s from TG’s to be used as fuel.

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7
Q

What does glucagon do in the skeletal muscle?

A

Nothing. There aren’t any receptors there.

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8
Q

Glucagon is released from where in response to what?

A

Glucagon is released from α-cells in the pancreas; its controlled by a reduction in glucose or a rise in blood insulin (bathing the α-cells).

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9
Q

What are some problems if you can’t control your glucose levels?

A

hyperglycemia (polyuria and polydipsia; if chronic may lead to glycosylation of proteins (distorts and slows degradation) such as Hba (diabetics) or hypoglycemia (fatigue, confusion, blurred vision, lightheadedeness, loss of consciousness, and coma).

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10
Q

What is the general structure of insulin?

A

Insulin is a polypeptide hormone that when active form is made up of 2 polypeptide chains (A &B) linked by 2 interchain disulfide bonds.

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11
Q

How does insulin get from a pre-hormone state to the active form?

A

Insulin is a polypeptide hormone made as a preprohormone and is converted into a proinsulin in the RER; the “pre” sequence (a short hydrophobic signal sequence at the N-terminal end) gets cleaved. The proinsulin then folds into the proper conformation and disulfide bonds are formed between the cysteine residues. It is then packaged into microvesicles (w/ zinc ions) that are transported to the golgi complex, where a protease removes the biologically inactive C-peptide; this produces the biologically active insulin.

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12
Q

How can the C-peptide of insulin provide a diagnostic tool for physicians?

A

Insulin and C-peptide are secreted from the β-cell in equal proportions, however the C-peptide is not cleared from the blood as rapidly as insulin. As a result, it provides a reasonably accurate estimate of the rate of the insulin secretion. This becomes useful when working with patients with Diabetes mellitus because the C-peptide allows the doctor to estimate degree of endogenous insulin secretion in patients who are receiving exogenous insulin, which lacks the C-peptide

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13
Q

What is the mechanism in which insulin is released form the pancreatic islet cells?

A

Glucose freely enters the cell –> goes through glycolysis –> ATP increases –> ATP-dependent K channels close –> membrane depolarizes –> Ca channels open –> vesicles containing insulin are released in the blood

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14
Q

What are the 4 stimulators of insulin release?

A

Glucose, amino acids, neural input, gut hormones.

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15
Q

What are the 4 stimulatants of glucagon release?

A

Amino acids, cortisol, neural input, epinephrine

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16
Q

What are the 2 inhibitors of insulin release?

A

Low glucose levels, epinephrine.

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17
Q

What are the 2 inhibitors of glucagon release?

A

Glucose and insulin

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18
Q

What and how does epinephrine affect metabolism?

A

It mobilizes fuels during stress by glycogenolysis in the liver and muscle and stimulates fatty acid release from adipocytes.

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19
Q

What and how does cortisol affect metabolism?

A

Provides for changing requirements over a long term. Stimulates muscle proteolysis, gluconeogenesis and lipolysis.

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20
Q

What type of receptor is the insulin receptor?

A

Tyrosine kinase

21
Q

What type of receptor is the glucagon receptor?

A

Gs-protein coupled receptor. Binding increases cAMP

22
Q

What type of receptor does cortisol act on?

A

Cortisol is s steroid hormone so it binds to intracellular receptors or binding proteins, which then (if not already) move into the nucleus so it can interact with chromatin. As a result this will change the rate of gene transcription in target cells.

23
Q

What type of receptor does epinephrine act on?

A

They act on Gs-protein coupled receptors. β1-receptor: Heart; NE. β2-receptor: Liver, skeletal muscle, and other tissues involved in mobilization of fuels. Epinehrine. α3-receptor: adipose tissue (fatty acid oxidation; and thermogenesis)

24
Q

What type of bond does sucrose have between the two sugar molecules?

A

α-1,2-glycosidic bond

25
Q

What type of bond does lactose have between the two sugar molecules?

A

β-1,4-glycosidic bond

26
Q

Sucrose is the combination of what 2 sugar molecules?

A

Glucose and fructose

27
Q

Lactose is e combination of what 2 sugar molecules?

A

Glucose and galactose

28
Q

What occurs during the digestion of carbohydrates by amylase in the mouth?

A

In the mouth salivary α-amylase (endoglucosidase) cleaves starch by breaking α-1,4 linkages between glucose residues within the chains –> shortened polysaccharide chains called α-Dextrins (linear and branched oligosaccharides) which enter the stomach. Salivary α-amylase is inactivated by acidity (HCl; parietal cells) in the stomach.

29
Q

What occurs during the digestion of carbohydrates in the duodenum?

A

The stomach contents pass into the intestine where HCO3- secreted by the pancreas neutralizes the stomach acid, thereby increasing the pH into the optimal range necessary for intestinal enzymes. Pancreatic α-amylase acts in the lumen of the small intestine cleaving the α-1,4 linkages between glucose residues. The products of pancreatic α-amylase are disaccharides maltose and isomaltase, trisaccharides, and small oligosaccharides containing α-1,4 and α-1,6 linkages.

30
Q

What do glucoamylases and maltases do on e brush border of the SI?

A

cleaves residues from the non-reducing ends of oligosaccharides and also cleave the α-1,4 bond of maltose, releasing 2 glucose residues. It has 2 catalytic sites with small differences in substrate specificity between the two, and it is heavily glycosylated to protect it from digestive proteases. Glucoamiylase activity increases progressively along the length of the SI, activity is highest in the ileum.

31
Q

What is the function of isomaltase on the brush border of the small intestine?

A

Isomaltase cleaves α-1,6 linkages, releasing glucose residues from branched oligosaccharides

32
Q

What is the function of sucrose on the brush border of the small intestine?

A

Converts sucrose to glucose and fructose

33
Q

Hwhat s the function of trehalase on the brush border of the small intestine?

A

Trehalase hydrolyzes the glycosidic bonds in trehalose (insects, algae, and fungi); its a discaccharide composed of 2 glucosyl units linked by and α-bond between their anomeric carbons.

34
Q

What are the symptoms of the lack of trehalase?

A

nausea, vomiting, and GI distress

35
Q

What is the function of lactase on e brush border of the small intestine?

A

Lactase (β-galactosidase) converts lactose to glucose and galactose; its activity is highest in the jejenum

36
Q

What is the major cause of adult lactose intolerance?

A

Adult hypolactasia is the normal condition for most of the world’s population. It can be due to low levels of lactase or it intestinal injury (disease) to the absorptive cells of the intestinal villi thereby diminishing lactase activity (secondary lactase deficiency)

37
Q

Lactose intolerance patients allow the bacteria to convert the lactose into what products?

A

Low levels of lactase allows the undigested lactose to be turned into lactic acid, methane, and H2 gas by bacteria. Lol farting.

38
Q

What type of bond does cellulose have that we can’t digest?

A

β-1,4 bonds

39
Q

What is the dietary benefit of eating indigestible carbohydrates like cellulose?

A

Dietary Fiber softens a persons stool –> lessens the pressure colon wall –> greater expulsion of feces (YES!!!!)

40
Q

What is the dietary benefit of eating pectins?

A

Pectins lower blood cholesterol levels by binding bile acids (help out people with diabetes mellitus by slowing the rate of absorption of simple sugars and preventing high blood glucose after meals)

41
Q

What is the dietary benefit of eating β-Glucans (oats)?

A

β-Glucan (oats) reduce cholesterol levels through a reduction in bile acid resorption in the intestine

42
Q

What I the glycemic index and why is it important?

A

The glycemic index measures how fast and how much a food raises blood glucose levels. This is especially important for diabetics, because it needs to be considered in order to properly maintain blood glucose levels. Consumption of a low-glycemic-index diet results in a lower rise in blood glucose after eating, which is easily controlled by exogenous insulin

43
Q

Which types of sugars have the highest glycemic index?

A

Glucose and maltose have the highest glycemic indices. But the glycemic response to ingested foods depends not only on the glycemic index of the foods but also on the fat and fiber content, but also the method in which it is prepared.

44
Q

What is the difference between GLUT1-5?

A
45
Q

What is the insulin sensitive GLUT and where is it found?

A

GLUT4- found on adipose ans skeletal muscle tissues

46
Q

What does insulin do to GLUT4 transporters?

A

In muscles and liver transport of glucose is stimulated by insulin. This involves the recruitment of GLUT 4 from intracellular vesicles into the plasma membrane. In adipose tissue insulin causes the synthesis of fatty acids and glycerol, and in muscle it increases glycolysis and glycogen synthesis

47
Q

How is the transport of glucose into RBC’s regulated?

A

glucose transport is not rate-limited even during fasting because GLUT 1 is present in very high concentrations

48
Q

How is transport of glucose into the liver regulated?

A

Km for GLUT 2 is pretty high as a result the liver will only store glucose when blood glucose levels are high

49
Q

How will glucose pass through the BBB?

A

passed through rapidly and taken up by GLUT1 and GLUT3 transporters.