Lecture 7 Part 2 Flashcards

1
Q

what is hypoglycemia

A

low blood sugar

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2
Q

nongluconegenic compounds

A
  • not efficient at making things
  • cannot be used to produce NET glucose
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3
Q

what are some nongluconegenic compounds

A
  • acetyl CoA
  • fatty acids
  • some amino acids
  • acetic acid
  • butyric acid
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4
Q

insulin

A
  • synthesized and secreated by pancreas
  • beta cells of the Islets of Langerhans
  • responds to high blood sugar
  • stimulates glucose uptake by muscle and adipose tissue
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5
Q

hormonal control of CHO metabolism

A

insulin

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6
Q

hormonal control of CH2O metabolism

A

glucagon

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6
Q

glucagon

A
  • synthesized and secreted by pancreas
  • alpha cells of Islets of Langerhans
  • responds to low blood sugar
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7
Q

what does glucagon stimulate liver to

A
  • glycogenolysis
  • gluconeogenesis
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8
Q

glucocorticoids

A
  • hormonal control of CHO metabolism
  • cortisol produced and released by adrenal gland
  • stimulated when blood sugar low or stress
  • stimulates gluconeogenesis
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9
Q

what are the side effects of glucocorticoids

A

immune, inflammation

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10
Q

epinephrine

A
  • hormonal control of CHO metabolism
  • produced and released by adrenal gland
  • stimulates glycogenolysis
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11
Q

ruminant carb metabolism

A
  • microbial fermentation of fiber and sugars
  • cellulytic bacteria digest hemicellulose and cellulose to VFA’s
  • alter proportion of VFA’s and lactate
  • feed additive to alter VFA’s
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12
Q

what are the end products of microbial fermentation of fiber and sugars

A

VFA’s + organic acids
- acetate
- propionate
- butyrate
- lactate
- 99% sugars converted to VFA’s

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13
Q

high forage diet=

A

acetate highest
propionate next highest
butyrate lowest

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14
Q

high concentrate diet=

A

acetate is lowered
propionate increased

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15
Q

acetate

A

TCA cycle
- used in muscle and adipose tissue

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16
Q

propionate

A
  • TCA cycle
  • metabolizes in liver to glucose
  • when feeding more carbs
17
Q

butyrate

A
  • TCA cycle
  • converted to glucose in liver
  • stay at more local level (rumen)
18
Q

lactate

A
  • converted to glucose in liver
  • potentially be substrate
19
Q

what is the primary VFA from cellulose and hemicellulose

A

acetate
- feeding a lot of fiber

20
Q

what is acetate necessary for

A

butter fat synthesis

21
Q

which VFA yields more glucose

A

propionate

22
Q

what are feed additives that alter VFA’s

A

rumensin
bovatec

23
Q

ionophore

A
  • an additive, technically an antibiotic
  • increases propionate
  • decreases production of acetate and butyrate
24
Q

what does an ionophore improve

A

energy efficiency
improves F/G
improves ADG

25
Q

what species are ionophores toxic to

A

horses

26
Q

ketosis

A
  • excess of ketones
  • seen when CHO intake is lower
  • cause lack of CHO or gluconeogenic AA derived precursors to oxalate
27
Q

what are the three types of ketones

A

acetone
acetoacetic acid
B-hydroxybutyric acid

28
Q

what is ketosis known as in ewes

A

pregnancy disease
- when carrying multiple lambs

29
Q

what does ketosis in ewes cause

A
  • decrease glucose
  • increase glucagon and epinephrine
  • death
  • lethargy
30
Q

as ketones increase,

A

appetite decreases

31
Q

what is the treatment for ketosis in ewes

A

does with propylene glycol to provide immediate source of energy
- prevent with feeding grain last 4 weeks

32
Q

what are the effects of ketosis in dairy cows

A
  • seen in early lactation
  • negative energy balance
  • poor appetite
33
Q

fat stores being metabolized=

A

elevated ketones

34
Q

how do you treat ketosis in dairy cattle

A

same as sheep
- propylene glycol
- increase grain in diet
- prevent with high energy, high fiber ration, and Rumensin

35
Q

diabetes mellitus types

A
  1. juvenile onset (type 1)
  2. adult onset (type II)
  3. gestational onset
36
Q

type 1

A
  • higher than normal blood glucose
  • usually autoimmune disorder
  • treatment= insulin injections
37
Q

what is type 1 diabetes caused by

A

underproduction of insulin by pancreas due to destruction of beta cells

38
Q

type II

A
  • higher than normal blood glucose
  • common in dogs
  • treatment= diet and exercise and weight control
39
Q

what is type II caused by

A
  • defect in insulin receptor mechanism at target tissue level
  • obesity
40
Q

gestational onset

A
  • higher than normal blood glucose and ketone levels
  • recovery is common after delivery
  • 2 to 5% of all pregnancies
41
Q

what causes gestational onset

A

increased tissue resistance to the action of insulin