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111 Cards in this Set

  • Front
  • Back

Different types of endocrine "glands"

-Single cells dispersed throughout a non-endocrine organ (gastrin cells)

-clusts of cells within a non-endocrine organ (pancreas)

-endocrine gland dedicated completely to endocrine function (pituitary)

-endocrine cells associated with meiosis and reproduction (ovaries)

Insulin synthesis

-synthesized as prohormone

-packaged in golgi and stored in secretory vessels with zinc

-C peptide is removed within vessel

-Insulin and C peptide are secreted

C peptide

fragment released with insulin. Can be used to assess beta cell function

Biphasic release of insulin

Initial burst of insulin followed by a slower long lived increase

Out of the pancreas, where does insulin reach first?

The liver via the portal vein

Glucose stimulated insulin secretion

-Glucose enters beta cell thru GLUT2

-Converted to G6P

-Glycolysis produces ATP

-ATP binds to ATP-regulated K channel and causes depolarization

-Voltage gated Ca channels open

-Ca promotes insulin secretion

GLP-1 stimulated insulin secretion

-GLP-1 from small intestine binds to GLP-1 receptor on beta cells

-Activates Gs

-Increases cAMP, PKA, and Ca

Long chain free fatty acid stimulated insulin secretion

-Bind GPR40

-Activate Gq

-Increase PKC and Ca

Norepinephrine stimulated insulin secretion

-Bind alpha 2 adrenergic receptor

-Activate Gi

-Decrease cAMP and Ca

-Decrease insulin secretion

Ach stimulated insulin secretion

-Bind muscarinic receptor

-Activate Gq

-Increase Ca

Insulin signaling pathway

-Insulin binds and induced conformational shift

-Cross-phosphorylation of cytoplasmic domaints

-Recruitment and phosphorylation of IRS

-PI3K recruited

-PIP2 converted to PIP3

-PK1 and AKT recruited

-AKT regulates protein phosphatases, FOXO1, mTORC1, and SREBP-1

Can also recruit SOS which activates Ras and MAPK cascade

Insulin resistance

Blocks IRS due to:

-Inflammatory cytokines

-increased intracellular triglycerides

-Increased amino acids activate mTORC1 which negatively feeds back

-Binding of SOCS3


Activated by insulin

Promotes protein synthesis

Can be activated by influx of amino acids

Activates SREBP1c

What happens when mTORC1 is high?

Feeds back to insulin receptor and IRS to decrease insulin signaling


Activated by insulin and AKT

Enters the nucleus and upregulates gene expression in hepatocyte

Upregulates glucokinase and pyruvate kinase, stimulating glycolysis

Upregulates PPP

Drives fatty acid synthesis

Protein phosphatases

Needed for glycogen synthesis, glycolysis, and entry of pyruvate into the TCA cycle


Important during fasting

Stimulates gluconeogenesis and assembly of VLDLs

What does insulin do to FOXO1

Phosphorylates it and inhibits it

What does PKC do to IRS

Inhibits it

How is glycogen synthase activated?

By dephosphorylation via protein phosphatases

How is the PPP activated?


What does insulin do to LPL?

Increases it

What does insulin do to VLDL?

Inhibits the assembly and secretion of VLDL from hepatocytes


Proteins that coat and stabilize fat droplets.

When phosphorylated, they release TGs from adipose stores

Which cells do not express glucagon receptors?

Skeletal muscle

Primary adrenergic receptor on beta cells

Alpha 2

Primary adrenergic receptor on alpha cells

beta 2


Activated by insulin/AKT signaling

Increases F26BP

Inhibits gluconeogenesis

How is glycolysis increased in the liver during a fed state?

Increased F26BP and PFK1

Increased pyruvate kinase (SREBP1C)

Increased pyruvate dehydrogenase

Decreased PEPCK

How is triglyceride synthesis increased in the liver during a fed state?

Excess AcCoA is converted to citrate and shuttled to the cytoplasm where is is converted back to AcCoA then to malonyl CoA and then to fatty acids

What does malonyl CoA do?

Inhibits beta oxidation

What happens in the liver during the fed state?

Increased glucokinase

Increased glycogen synthase

Decreased glycogen phosphorylase

Increased glycolysis

Increased triglyceride synthesis

Decreased gluconeogenesis

How does the liver increase glycogenolysis during fasting?

Increased glycogen phosphorylase

Decreased glycogen synthase

How does the liver decreased glycolysis during fasting?

Decreased pyruvate kinase

Decreased F16BP and G6Pase

How does the liver increases gluconeogenesis during fasting?

Increased PEPCK

How does the liver decrease lipogenesis during fasting?

Increased malonyl CoA decarboxylase

What happens to skeletal muscle during the fed state?

Increase glucose uptake via GLUT4

increase glycolysis

Increase glycogen synthesis

Increase protein synthesis

Increase lipogenesis (in extreme excess)

What happens to adipose during the fed state?

Increase lipoprotein lipase

Increase FFA storage

Increase glucose uptake via GLUT4

Decreased hormone sensitive lipase

Increase protein synthesis

What happens to adipose during fasting?

Activation of hormone sensitive lipase

Phosphorylation of perilipins to release TGs

Beta oxidation of FFA

Ketone bodies formed from AcCoA

Loss of GLUT4


What happens to skeletal muscle during fasting?

Decreased GLUT4 and glycolysis

FFAs and ketone bodies used for ATP

Muscle-specific LPL releases FFAs from VLDL

Gluconeogenic substrates released

Muscle glycogen used during exercise

AMP kinase

During caloric deprivation, exercise, or activation of sirtuins, the ration of AMP to ATP increases.

This activates AMP kinase which increases catabolic reactions in the cell and decreases anabolic reactions


Cells package their organelles into vaculoes that fuse with lysosomes and degrade them for ATP

GCN2 pathway

GCN2 senses low amino acid levels in tRNA and inhibits protein synthesis.

Also stimulates amino acid synthesis and inhibits lipid synthesis

What does AMP kinase do to mTORC1?

Inhibits it

Abnormal mTORC1 activation

Mutated TSC1/2

Leads to tumors in the CNS, seizures, and mental retardation


When there is too much energy in a cell, too many proteins are made and not folded correctly.

UPR detects the unfolded proteins and increases the expression of anti-oxidant genes and inflammatory genes to protect the cell.

It also decreases protein synthesis and increases TG synthesis.

If all else fails, apoptosis will be induced

Anorexigenic peptide

Senses when the stomach is full

Ex: serotonin, alpha MSH, catecholamines, CCK, GLP-1, insulin

Orexigenic peptide

Senses when the stomach is empty

Secreted when Ghrelin is perceived

Ex: neuropeptide Y, cannabinoids


Inversely proportional to fat mass. Inhibits food intake by increasing insulin sensitivity


Encourages the use of calories so we don't increases adipose reservoir. Signals there are adequate fat stores.

Secreted proportional to fat mass

Stimulates angiogenesis, humoral and adaptive immunity, steroid synthesis. Decreases insulin secretion.

Neuropeptide Y

Stimulates food intake

Alpha MSH

Necessary for leptin to work since leptin does not act directly on output neurons.

Inhibits food intake and stimulates ATP use


Stimulate food intake and converse ATP

Leptin deficiency results in

Morbid obesity

What may cause resistance to diet-induced weight loss?

UCP protein mutation

Adrenergic receptor mutation

Parathyroid hormone

Functions to increase plasma Ca

Increases bone resorption

Increases Ca reabsorption in kidney

Decreases Pi reabsorption in kidney

Activation of CaSR

Inhibits PTH secretion

Degrades newly synthesized PTH

Vitamin D

Stimulates Ca and Pi absorption in small intestine by upregulating TRPV5/6 and calbindin

Facilitates Ca reabsorption in kidney

Helps out PTH

Synthesis of Vitamin D

Aquired from UV radiation and the diet

Hydroxylated in the liver

Hydroxylated in the kidney (rate limiting step)

Stimulated by PTH and inhibited by high levels of Pi

Transported by vitamin D binding protein

Vitamin D deficiency

Causes Ca and Pi to fall and prevents proper mineralization of bone.

Rickets in children and osteomalacia in adults


Synthesized and secreted by parafollicular cells of thyroid

Stimulated by high plasma Ca

Inhibits bone reabsorption


Produced by osteocytes

Needs to be inhibited

Excess causes an inhibition of Pi reabsorption in the kidney and inhibition of Vit D hydroxylation in the kidney. Leads to hypophosphatemia and bone wasting

Ca transport in thick ascending limb

Triple transporter drives Ca transcellularly

Positive lumen drives Ca paracellularly

CaSR on basolateral side can detect high Ca and inhibit the triple transporter

Ca transport in collecting duct

Ca enters thru TRPV5 and is shuttled transcellularly and exits thru Na/Ca exchanger

PTH acts here to upregulate TRPV5

Pi transport in proximal tubules

80% occurs here

Uptake via Na/Pi symporter NPT2 and exits thru Pi/anion exchanger

PTH causes apical transporter to be internalized and degraded

PTH effects on Ca and Pi in the kidney

Promotes Ca reabsorption in DT and TAL

Inhibits Pi reabsorption in PT

PTH or Vit D on bone

Binds to osteoblast and activate RANKL

Stimulates of osteoclast differentiation

Blocked by OPG

Formation of thyroid hormone

Na/I symporter on thyroid follicle cells

Iodide is transported to the lumen

Tyrosine is iodinated by thyroid peroxidase

Dual oxidase generates hydrogen peroxide

Colloid droplets are internalized and hydrolyzed

T3 and T4 are secreted

Thyroid regulation

T3 feeds back to the pituitary

Pituitary can convert T4 to T3 so it can participate in the feedback

Some feedback to the hypothalamus, but minimal

What happens with high levels of T4

TSH is suppressed


Activates Gs and Gq to upregulate Na/I symporter and take up more iodide

Increases dual oxidase and peroxidase

Upregulation of thyroglobulin transcription

Gland can become hypertrophic and hyperplastic

What happens when intrathyroidal iodide concentrations are very high?

Thyroid hormone synthesis and secretion is inhibited

Dual oxidase and peroxidase are inhibited

Thyroid hormone transport

Bound to TBG, TTR, or albumin

T4 binds more avidly

T4 conversion

T4 is a prohormone and must be converted to T3 to be used

D1 in liver and kidney (supplies serum T3)

D2 in brain, pituitary, brown fat (local generation)

Euthyroid sick syndrome

Decreased T3 or T4 seen with chronic illness even though the thyroid is working fine

D1 and D2 are inhibited


inactivates T3 and T4

makes reverse T3

Actions of thyroid hormone

Bone growth and differentiation

Brain function and differentiation

Beta adrenergic agonist

Increases ATP use but decreases efficiency (heat production)

How thyroid hormones generate heat


Increase Na/K ATPase pumps

Promote futile cycles

insert uncoupling proteins into the mito membrane

TR alpha

Found in brain, heart, kidney, bone

Regulate growth, body temp, post-natal differentation, heart rate

TR beta

Found in hypothalamus, pituitary, choclea, liver

Negative feedback in HPT axis

Lowers cholesterol and TG

GH signaling

GH binds and causes receptor dimerization

Bring JAK2 together

Trans phosphorylation of JAK2

Docking site for STAT5b

Moves to the nucleus and activates IGF-1 transcription

Inhibited by SOCS


Important for both the growth of the fetus and the placenta during fetal life

Paternally expressed gene

GH in the fed state

Amino acids promote GHRH release

Promotes growth and protein anabolism

Increases IGF-1

GH in the fasting state

Hypoglycemia promotes GHRH release

Switched fuel consumption to lipids by stimulating hormone sensitive lipase

Stimultes gluconeogenesis

Inhibits GLUT4 in muscle

Decreased IGF-1

GH axis

Hypothalamus produces GHRH

Pituitary produces GH (pulsitile release)

GH acts on the liver to produce IGF-1

IGF-1 feeds back to pituitary and hypothalamus

Ghrelin also stimulates the hypothalamus

Overall effect of GH

Decrease fat mass and increase muscle mass


Stimulated by GH

Forms a ternary complex in the liver. Acts as an endocrine hormone

Can act as via paracrine in the tissues directly

PTH effect on IGF-1

Stimulates it

Glucocorticoid effect on IGF-1

Inhibits it and slows growth

Precocious puberty

Early acceleration of linear growth and early closure of the growth plates. Leads to short stature

Larson dwarfism

Mutation in GH receptor, IGH-1 production in the liver is impaired


Promotes longitudinal bone growth and periosteal apposition

Closure of growth plates at the end of puberty

Maintains adult bone madd

Adrenal medulla

80% epinephrine

20% norepinephrine

How is epinephrine made?

Tyrosine (tyrosine hydroxylase) DOPA (aa decaroxylase) Dopamine (beta hydroxylase) NE (PNMT) Epi

Secretion of epinephrine

Sympathetic signals. Ach is released and binds to nicotinic receptors on chromaffin cells and increases tyrosine hydroxylase

Epinephrine promotes

glucogenolysis via beta 2 receptor. Increases blood glucose

Inhibits insulin secretion via alpha 2

Epinephrine degradation

MAO and COMT to metanephrine or vanillylmandelic acid and excreted in the urine

Zona fasciculata

Makes cortisol

biosynthesis of cortisol

Cholesterol (CPY11A1) pregnenolone

(3BHSD) pregesterone OR (CPY17) 17-hydroxypregnenolone

(CPY17) 17-hydroxyprogesterone OR (3BHSD) 17-hydroxyprogesterone

(CYP21) 11-deoxycortisol

(CPY11B1) cortisol

Cortisol inactivation

Inactivated in the liver or converted to cortisone by 11BHSD2

Cortisol binding

GR receptor is bound to chaperone in the cytoplasm

Binding of cortisol brings the complex to the nucleus and increases transcription


Transports free cholesterol into the inner mitochondrial membrane so it can get to CYP11A1

Physiological actions of cortisol

-Increases gluconeogeneis

-Decreases GLUT4 uptake

-potentiates PNMT and catecholamine lipolysis

-Increases muscle proteolysis

-Increases erythropoietin synthesis

-inhibits immune response

-decreases reproductive axis

-decreases inflammatory cytokines

-decreases collagen and fibroblast proliferation

-Decreases ADH

-Induces Type II pneumocyte differentiation


ACTH receptor on cells in zona fasciculata

Chronically elevated cortisol

-increased appetite

-increased glycogen synthesis

-decreases lipolysis

-Increased TG synthesis

-Truncal adiposity

Zona reticularis

Makes androgens (DHEAS)

Appears at age 5

Contributes 50% of active androgens in women

DHEAS biosynthesis

Pregnenolone (CPY17) 17-hydroxypregnenolone (CPY17) DHEA (SULT2A1) DHEAS

Regulation of DHEAS

Regulated by ACTH

Androgens don't feed back on CRH or ACTH. This loophole can give rise to congenital adrenal hyperplasia

Zona glomerulosa

Makes aldosterone

Aldosterone biosythesis

Pregnenolone (3BHSD) progesterone (CYP21B) 11-deoxycorticosterone (CYP11B2) Corticosterone (CYP11B2) Corticosterone (CYP11B2) 18-hydroxycorticosterone (CYP11B2) aldosterone

Actions of aldosterone

Increases Na reabsorption in the kidney and the colon

Increases ENaC

Increases ROMK

Proinflammatory and profibrotic effects on the heart causing LV hypertrophy