Endocrine

Hormone structure and action: describe general hormone synthesis, secretion, metabolism, and excretion

•Can be cyclical (rise and fall with sleep/wake cycle) •Negative feedback control •Metabolized by kidneys and liver; degraded by target cell after binding to receptors (excreted from system when we don't need them anymore)

Hormones: Hyperresponsiveness

•Depressed cell response or resistance to hormone (tissue resistance- similar to hyposecretion) •Typically caused by lack of or a deficiency in cell receptors, but can occur with postreceptor mechanisms (second-messenger dysfunction that causes decreased cellular response) •Hormone resistance of the target tissues will cause the same set of clinical symptoms as hyposecretion.

Hormones: Hypersecretion (descriptive outline of primary vs. secondary)

•Excess secretion of hormone (secreting tumors, autoimmune, excessive stimulation from trophic signals) •Primary hypersecretion occurs when there is a dysfunction of the endocrine gland that results in abnormally high secretion of hormone. •Secondary hypersecretion occurs when there is an elevation in the tropic level of one hormone that results in an increased plasma concentration of another hormone.

Outline of insulin phases/actions

•First Phase: Brief rise in insulin from ingestion of glucose in food •Second Phase: Continued glucose causes insulin secretion •Incretin Effect: Insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) from cells in gut released •GIP and GLP-1 stimulate insulin production •GLP-1 inhibits glucagon •Insulin --> glucose into adipose and muscle tissue --> inhibits production of glucose by liver (glucose is stored as glycogen in the liver) •Glucose oxidized in the cell (glycolysis) and used primarily for glycogenesis (production of glycogen in liver and muscle)

hypersecretion of aldosterone: manifestations

•HTN, hypervolemia (increase of water), hypokalemia (increase of aldosterone leads to increased excretion of potassium)

Hypersecretion of parathyroid hormone: manifestations

•High serum calcium!! •Kidney stones, osteoporosis (result of bone breakdown; PTH pulls calcium from bones), bradycardia, heart block, cardiac arrest •High Ca decreases neuromusc excitability

What are the categories of endocrine diseases?

•Hyposecretion •Hypersecretion •Hyporesponsiveness of target cells

Normal lab levels of urinalysis

•Look for ketones in urine if glucose >300 or pregnant, ill, or ketoacidosis suspected Increased sugar = overwhelmed transporters leading to glucose in urine

Hyposecretion of parathyroid hormone: manifestations

•Low serum calcium!! •Circumoral numbness, paresthesia of extremities, muscle cramps/spasm (Cvostek or Trousseau sign), fatigue, anxiety, prolonged QT Cvostek- Tap facial muscles, same side of face will contract -"cheek stick" Trousseau- More sensitive BP cuff inflated x 3 min, hand and forearm flex

Trends with DM

•Number of diagnosed and undiagnosed people with diabetes continues to rise •Costly to healthcare system Those with diabetes at increased risk for: •Blindness •Renal failure •Heart Disease •Amputation •Pregnancy complications

Normal function of organs and hormones (insulin and glucose, non-diabetics)

•Remember, glucose needs a transporter (GLUT1-4) to get into the cell! •Insulin is the key that unlocks this transporter to come to cell surface Glucose transporters (GLUT1 to 4) are specific to each tissue -Neurons and erythrocytes (GLUT1) do not require insulin -Heart, adipose, and skeletal muscle cells require insulin and activate glucose transporters (GLUT4) -in order to maintain homeostasis, these tissues require glucose (therefore, requiring glucose transporters) •Insulin is synthesized in the pancreas by the β (beta) cells of the islets of Langerhans •α (alpha) cells produce glucagon

Explain Receptor Specificity and Affinity (and permissiveness, good to know ig)

•Specificity: molecular "fit" of a hormone within a receptor binding pocket •Affinity: degree of "tightness" of the hormone-receptor bond, or the inclination of the hormone to remain bound to the receptor Affect the potency of the hormone and whether the cell will respond "Cross-specificity" may occur between hormones. Permissiveness •Hormones can increase the number of receptors for other hormones, thus enhancing the effect of the second hormone. •Allows cellular events to occur in sequence (i.e., estrogen secreted early in the menstrual cycle causes increase in the number of uterine receptors for progesterone)

Hormones of the Hypothalamus and Anterior Pituitary Gland (general overview of how they work together)

•Three-tiered axis: hypothalamic releasing and inhibiting hormones, anterior pituitary hormones, and target organ hormones •All hypothalamic releasing and inhibiting hormones are peptides, with the exception of dopamine, and all are water soluble -Growth Hormone (GH), Prolactin, Gonadotropin, Thyroid Stimulating Hormone (TSH), Adrenocorticotropic hormone (ACTH)

Hormones: Hyposecretion (descriptive outline of primary vs. secondary)

•Too little secretion of hormone (congenital, absence of gland, autoimmune destruction, surgical removal, lack of normal trophic signals) •Primary hyposecretion occurs when an endocrine gland releases an inadequate amount of hormone to meet physiologic needs. •Secondary hyposecretion occurs when secretion of a tropic hormone (hormones that stimulate other glands, such as the ones released from the anterior pituitary) is inadequate to cause the target gland to secrete adequate amounts of hormone.

Peptide hormones

•contained within lipid bilayer of the vesicles and stored until a trigger results in exocytosis of the hormone into the extracellular space

Catecholamines (how are they formed?)

•formed by enzymes within the cytoplasm that begin with tyrosine and through a series of steps convert it to dopamine, norepinephrine, or epinephrine

How are thyroid hormones formed?

•synthesis precedes secretion by weeks or months in the thyroid follicle and bound to protein thyroglobulin; secretion occurs via cleavage of the thyroid hormone based on systemic needs determined by the hypothalamus and pituitary gland

Hyposecretion of cortisol (etiology and manifestations, long af)

-Adrenocortical disorder Etiology, pathogenesis, population/cause: -Addison's you need to Add hormones (cortisol) -Primary: hyposecretion caused by adrenal cortex disease (Addison) -Secondary: decreased secretion of ACTH (r/t corticosteroid tx and withdrawal) (problem with trophic gland needed to release ACTH) -Congenital: adrenal hyperplasia -Pedes (congenital adrenal hyperplasia- rare) and adult Manifestations -Anorexia, weight loss, weakness, hypoglycemia, hyperkalemia (decreased cortisol leads to decreased aldosterone, therefore increase of potassium), diminished vascular tone-> low BP (circulatory collapse) •Severe: Addisonian crisis (risk of severe intravascular collapse)

Growth Hormone (GH)

-Affects metabolic processes by increasing muscle mass and decreasing fat mass -Primary target organ is the liver -Increased GH leads to increased glucose -Cyclic (rises after sleep) -Normally, metabolic functions (protein, muscle growth, skeletal growth, cartilage growth)

What are the actions of insulin?

-Enhance protein synthesis and prevent muscle breakdown -Inhibit gluconeogenesis -Enhance fat deposition by preventing fat breakdown (lipolysis) and inducing lipid formation -Stimulate growth by enhancing secretion of IGF-1 (somatomedin)

Adrenal medulla hormones (types and purpose)

-Epinephrine and norepinephrine -Released in response to SNS activation -Increase HR, contractility, skeletal muscles

Glucose metabolism during exercise (outline)

-Exercise increases insulin sensitivity (we need less insulin release with increased exercise) -Decrease glucose with less effort 1. Insulin levels drop, glucagon and catecholamine levels rise, stimulating glycogenolysis (FFA) 2.Glucose from liver meets energy demands 3. Muscle contractions increase insulin sensitivity, therefore normal blood glucose levels are maintained even with lower insulin

Antidiuretic Hormone

-Hormone secreted by the posterior pituitary gland to prevent the kidneys from expelling too much water -Cause water retention by reabsorption by renal collecting duct in response to concentrated body fluids and hypotension -Conserves water in the body, creates concentrated urine, and reduces serum osmolality

Calcitonin: purpose and mechanism of release

-Increases bone formation by osteoblasts and inhibits bone breakdown by osteoclasts -Decreases blood calcium and promotes conservation of hard bone matrix

Addisonian crisis

-Manifestation of hyposecretion of cortisol -Severe hypotension and vascular collapse

Oxytocin

-Released from posterior pituitary -Love and labor hormone -Released during sexual activity, childbirth, breast feeding

Aldosterone (role in long-term BP control)

-Renin from kidney converts angiotensinogen to angiotensin 1 in the blood vessels, then angiotensin-converting enzyme (ACE) converts angiotensin 1 to angiotensin 2 in the lungs, then angiotensin 2 from the lungs stimulates release of aldosterone from adrenal cortex

lipid soluble hormones

-act on intracellular receptors that directly activate genes -can enter cell -Remember- things that move through the cell membrane are lipid soluble, non-ionized- carried by transport proteins Intracellular receptors because can move through membranes -Steroid and thyroid hormones

Prolactin

-gestation -stimulates milk production and breast tissue development

Thyroid Stimulating Hormone (TSH)

-stimulates secretion from thyroid gland -bind to TSH receptors in thyroid gland and regulate thyroid function

Acute signs of hyperglycemia

3 P's •Polyuria (increased urine) •Polydipsia (increased thirst) •Polyphagia (increased hunger) •Nausea •Fatigue •Blurred Vision •More prone to infections

What are the posterior pituitary hormones?

ADH and oxytocin

Glucose metabolism during stress (physical or psychological)

Basically, an increase of stress hormones decreases glucose uptake in cells (happens with patients that don't have diabetes as well) 1. Stress hormones increase gluconeogenesis and glucagon; decrease utilization of glucose 2. Catecholamines increase production of FFAs and inhibit glucose uptake by peripheral cells 3. Stress hyperglycemia

Review of normal metabolism of glucose

Basically, eat sugar, then insulin is secreted by pancreas (beta cells) for the tissue cells to use glucose 1. Glucose Consumed in Food (main source of energy in the body) 2. Insulin secreted by pancreas helps body cells convert glucose to fuel (Type 1 DM: no insulin; Type 2 DM: can't use insulin effectively; insulin resistance) 3. Cells use glucose for energy metabolism (diabetes: hyperglycemia)

Glycogenolysis

Breakdown of glycogen to make glucose (Destruction!)

Etiology of endocrine disorders

Congenital Autoimmune Neoplastic Functional Tissue Resistance Iatrogenic Primary vs. Secondary From notes in powerpoint: Congenital: Inborn genetic defect that causes excessive production of hormone precursors Autoimmune: Involves genetic predisposition and environmental trigger; antibodies made against antigens on self-tissue cells (Graves disease) Neoplastic: Hormones may be produced by abnormal tissue sites (ectopic) such as malignancies (ex. Squamous cell carcinoma lung cancers make SIADH) Functional: Caused by nonendocrine disease such as chronic renal failure, liver disease, or heart failure (ex. CRF decreased EPO) Tissue Resistance: Occurs when target tissue fails to respond to a hormone (hormone resistance or target tissue resistance) Iatrogenic: Induced by medical treatments such as chemotherapy, radiation therapy, or surgical removal of glands ØTreatment for endocrine hyperfunction involves removal or destruction of glandular tissue with resultant chronic hypofunction. •Chronic hormone replacement therapy may be required (ex need levothyroxine/Synthroid after thyroid gland removal) Primary vs secondary just talked about: need lab results to know which gland is dysfunctional: Primary: dysfunction of hormone producing gland (gland failure, low levels of circulating hormone, blood levels of corresponding trophic hormone elevated) Secondary: abnormal pituitary secretion of trophic signals (pituitary doesn't release trophic hormone and gland production low so both levels low)

Hormone structure and action: describe receptor responses in terms of specificity and affinity

Control number of receptor sites via upregulation and downregulation -specific for certain receptor sites and attraction for such receptor sites Upregulation: Chronically low hormone concentrations cause increase in number of receptors (cells more sensitive to hormone) -allow for maximum amount and action of receptor sites Downregulation: Prolonged high hormone concentrations cause decrease in number of receptors •The ability of a cell to respond to a particular hormone depends on the presence of specific receptors for that hormone on or in the cell. •Target cells are able to regulate their responsiveness to hormones by altering the receptor number, affinity, and efficiency of coupling to intracellular responses.

Other than insulin, which hormones augment glucose production?

Corticosteroids, GH, catecholamines

Hypersecretion of cortisol (manifestations)

Cushings (hypercortisolism) •"Moon face" (round face, flushed cheeks) •Weight gain, thin extremities •Cervical fat pad (Buffalo hump), muscle weakness, hyperglycemia -abnormal metabolism of fat

Hypersecretion of cortisol (etiology and pathogenesis)

Cushings: •high cortisol- Cushion of steroids •Primary: ad. Cortex disease •Secondary: increased ACTH •Steroid Use

Hyposecretion of ADH

Diabetes Insipidus Etiology, pathogenesis, population/cause •Insufficient ADH Activity •Damage to hypothalamus or pituitary gland. -not holding onto enough water -constantly losing/peeing urine Manifestations •Polyuria & polydipsia (hallmark!) •Low urine SG (dilute) •Hypernatremia (seizure risk!!) •Lethargy •Seizures- neuron dehydration (concerning, dehydrated cells lead to seizures)

Hyposecretion of cortisol (etiology andpathogenesis)

Etiology and pathogenesis -Primary: hyposecretion caused by disease of adrenal cortex; idiopathic or autoimmune (Addison disease), surgical removal -Secondary: inadequate secretion of ACTH; usually iatrogenic, related to corticosteroid therapy (suppresses ACTH) Sudden withdrawal of corticosteroids -Tertiary: hypothalamic malfunction/injury Cortisol insufficiency is most clinically relevant -Congenital adrenal hyperplasia: rare cause in pediatric populations, because of specific enzymatic defects in the biosynthesis of cortisol by the adrenals Causes severe and life-threatening symptoms

Thyroid hormone hyposecretion: etiology, pathogenesis, population/cause

Etiology, pathogenesis, population/cause •Most are primary (Irradiation/removal of thyroid) •Secondary from hypo TSH secretion (head injury) •Hashimoto •Irradiation/removal •Surgical removal of the thyroid •Iodine deficiency •Infants (congenital), children and adults

Thyroid hormone hypersecretion: etiology, pathogenesis, population/cause

Etiology, pathogenesis, population/cause •Thyroid destruction releases T3/T4 (Hashimoto) •Primary: Graves (autoimmune-constant release) •Secondary: TSH receptors stimulated by TSH •Exopthalmos (protrusion of eyeballs; autoimmune response)

Purpose and normal lab levels of POC blood glucose

Finger stick -Immediate determination of glucose levels •<170 desirable •Or Glucose value in the lab

What are all anterior pituitary hormones?

Growth Hormone (GH), Prolactin, Gonadotropin, Thyroid Stimulating Hormone (TSH), Adrenocorticotropic hormone (ACTH)

Describe the half-life of hormones

Half-life -duration of hormone activity in circulation; expressed in minutes, hours, or days -the time for a hormone to reach one-half of its original concentration in the blood and is influenced by the rate of uptake by cells, degradation, and excretion. Lipids usually have a longer half-life.

Normal lab levels of HbA1c

HbA1c = glycosylated hemoglobin •Measure of long-term glycemic control -100-120 days (about 4 months) -<7% desirable

What do hormones regulate?

Hormones regulate complex functions including reproduction, growth/development, fluid homeostasis, and metabolism.

hypersecretion of aldosterone: etiology, pathogenesis, population/cause

Hyperaldosteronism •Primary: aldosterone secreting tumor •Secondary: low kidney perfusion stimulates RAAS •Aldosterone secreting tumors or low kidney function -too much sodium means too much water

Hypersecretion of parathyroid hormone: etiology, pathogenesis, population/cause

Hyperparathyroidism •Despite elevated Ca levels, PTH still secreted •Bone resorption and formation rates increased •Usually malignant cells that release PTH-like hormones cause hypercalcemic crisis

Adrenal medulla disorders: hypersecretion (etiology, pathogenesis, populatipn/cause)

Hypersecretion = Pheochromocytoma -increase of epinephrine and norepinephrine •Adrenal medulla tumor: •Catecholamines secreted in response to SNS stim (excess)

Adrenal medulla disorders: hypersecretion (manifestations)

Hypersecretion = Pheochromocytoma •HTN, tachycardia, headache, tremor, orthostatic hypotension, fever/weight loss -direct effect on medulla leads to hypersecretion of epi and norepi -Catecholamines increase heart rate, blood pressure, and glucose release from the liver.

Hypersecretion of cortisol

Hypersecretion: Hypercortisolism •Cushing: high cortisol •Primary: adrenal Cortex disease •Secondary: increased ACTH •Adenoma in pituitary (or tumor elsewhere) causes excess production of ACTH •Steroid Use •Steroid users •Those with tumors of pit. Or ad. cortex -Exogenous steroid use is the most common cause of Cushing syndrome in the United States.

Hyposecretion of parathyroid hormone: etiology, pathogenesis, population/cause

Hypoparathyroidism •Idiopathic or Autoimmune •Secondary: PT or Thyroid surgery •Can be temporary or permanent •Congenital lack of PT tissue •Adults or Infants (Surgery, Autoimmune, Congenital)

Parathyroid hormone: purpose and mechanism of release

Increases serum calcium levels in the blood -Detect serum Calcium concentration and help regulate levels through calcium absorption and reabsorption from bone -Decrease in Calcium causes PTH release -Elevated Calcium causes PTH suppression Acts on bones, intestine, and renal tubules to increase calcium levels In bone, increases osteoclastic activity (releases calcium into extracellular fluid) Increases renal calcium reabsorption Increases phosphate excretion by the kidney

Thyroid hormone hypersecretion: manifestations

Manifestations •Insomnia, restlessness, tremor, irritability, heat intolerance, enlarged thyroid (Goiter), weight loss (overmetabolism and increased O2 demand) •Severe: Thyroid Storm (medical emergency where the body is unable to meet the extreme demands of tissues)

Thyroid hormone hyposecretion: manifestations

Manifestations •Lethargy, cold intolerance, bradycardia, weight gain, dry skin •Severe: Myxedema Edema, decreased LOC, hypotension, hypothermia

Adrenal hormones (cortex and medulla description)

Medulla -sympathetic NS activation via epinephrine and norepinephrine Cortex (steroids from the cortex) -Glucocorticoids (cortisol) -Mineralocorticoids (aldosterone) -Sex steroids (androgens)

Describe negative feedback control of hormones and think of an example

Negative feedback control—some aspect of the secreted hormone is sensed and regulates further secretion •Example: body senses a need for the hormone, hormone is released; increase in hormone concentration exerts an inhibitory effect, or negative feedback, on further secretion of the hormone -Release of TSH once low levels of thyroid hormones (T3 and T4) sensed, TSH tells thyroid to release T3 and T4 •Maintains hormone activity within a normal range or set-point of normal activity

What are the different signaling paths that hormones use to regulate functions?

Neurocrine Endocrine Paracrine Autocrine

Adrenal Insufficiency (feedback with adrenal insufficiency)

Primary adrenocortical insufficiency (decreased cortisol production) leads to hypersecretion of adrenocorticotropic hormone (ACTH) because of lack of negative feedback. ACTH binds to receptors on melanocytes and stimulates pigment development in the skin. Even though ACTH levels are high, the adrenal gland is unable to produce adequate levels of cortisol.

Negative Feedback Loop: Primary vs Secondary Endocrine disorders

Primary: Breakdown of primary structure (ex. thyroid) resulting in inability to sense stimulations (ex. TSH) to release hormones (ex. T3 and T4) Secondary: Trophic structure abnormalities (ex. anterior pituitary), where they cannot release stimulating hormones to the primary hormone-secreting structures (ex. TSH release to signal thyroid gland)

Adrenal cortex hormones (types and purpose)

Purpose of all Made from cholesterol; lipid soluble. Regulate stress response. Activities regulate "The # S's: sugar, salt, sex". Aldosterone (mineralocorticoids): RAAS: maintain salt and water balance (Na retention, K excretion) -reabsorption of sodium (water follows, BFFssss) •Remember RAAS! •Released in response to low BP, low renal perfusion and high serum K •Aldosterone: released in response to angiotensin 2 (RAAS); maintain salt and water balance (Na retention, K excretion) Cortisol (glucocorticoids): -Oppose insulin; raise BS by increasing glucose uptake in cells and increasing glycogenolysis and gluconeogenesis -Protect against the damaging physiologic effects of stress and regulate the inflammatory and immune responses -Increases plasma glucose -Regulates immune and inflammatory reactions -Inhibits bone and collagen synthesis -Vital hormone in response to acute stress Androgens: (DHEAS) released in response to ACTH

What does the adrenal cortex synthesize?

Remember! Adrenal cortex synthesizes: Glucocorticoids -Cortisol is primary glucocorticoid and negative feedback suppresses adrenocorticotropic hormone (ACTH) release. Mineralocorticoids -Aldosterone regulated by the presence of angiotensin II Androgens -Sex hormones

Hypersecretion of ADH

SIADH Etiology, pathogenesis, population/cause: •Excessive ADH production •Stimulates renal tubules to reabsorb water despite decreased blood osmolality •Ectopic tumors producing ADH (lung malignancies) Manifestations: •Hyponatremia (low sodium, cell swelling) •Weakness •Muscle cramps •Confusion •Seizures- neuron swelling •Coma •High urine osmolality •Low serum osmolality

Adrenocorticotropic hormone (ACTH)

Stimulates adrenal cortex to secrete glucocorticoids -stimulates production of cortisol and adrenal androgens

What are the stress hormones?

Stress hormones=corticosteroids and catecholamines

What are the thyroid hormones and the purpose of each one?

T4 & T3 -Increase metabolic rate -Essential for growth and development (for children) -Regulated by TSH -Metabolism of fat, protein, and carbs/glucose T4 -90% cellular enzymes cleave an iodide molecule from T4 to transform into T3 (main circulating thyroid hormone) -circulates in plasma protein-bound to thyroid-binding protein T3 -10%; free in plasma and can cross directly into target cell -more active form of thyroid hormone

Thyroid hormone abnormalities: TSH and distinguishing primary vs secondary

TSH helps distinguish primary (low TSH) from secondary (high TSH).

Growth Hormone (GH) hyposecretion: etiology, pathogenesis, population/cause

Usually presents early in life Etiology, pathogenesis, population/cause -Decreased GH secretion -Defective GH action (abnormal receptor) -Defective IGF-1 (protein that synthesizes GH release is malfunctioning)

Growth Hormone (GH) hypersecretion: etiology, pathogenesis, population/cause

Usually presents early in life Etiology, pathogenesis, population/cause -Increased GH secretion from the pituitary gland -Tumor -Stimulates the liver to make IGF-1

Growth Hormone (GH) hypersecretion: manifestations

Usually presents early in life Manifestations -Hyperglycemia -Gigantism (kids) (increased linear growth) -Acromegaly (adults) (thickening of frontal sinus) -Enlarged organs

Growth Hormone (GH) hyposecretion: manifestations

Usually presents early in life Manifestations -Hypoglycemia (decreased glucose) -Decreased growth/muscle mass -Delayed puberty

gigantism

a condition produced by hypersecretion of growth hormone during the early years of life

Thyroid Storm

a relatively rare, life-threatening condition caused by exaggerated hyperthyroidism -Life-threatening thyrotoxicosis that occurs when excessive amounts of thyroid hormones are acutely released into circulation -medical emergency where the body is unable to meet the extreme demands of the tissues Thyroid Storm: Clinical manifestations Elevated temperatures, tachycardia, arrhythmias, congestive heart failure Extreme restlessness, agitation, and psychosis Precipitating event: stress, gland manipulation

Hashimoto's disease

an autoimmune disease in which the body's own antibodies attack and destroy the cells of the thyroid gland -etiology of hyposecretion of thyroid hormones

Graves disease

an autoimmune disorder that is caused by hyperthyroidism and is characterized by goiter and/or exophthalmos

Gonadotropins

anterior pituitary tropic hormones, follicles stimulating hormone (FSH) and luteinizing hormone (LH) which stimulate the gonads (ovaries and testes) to produce gametes and to secrete sex steroids -stimulate testosterone in men and estrogen and progesterone in women -pubertal changes with menses

water soluble hormones

bind to receptors on the surface of the cell -Extracellular target receptors unless special transport inside cell membrane -Peptide hormones and catecholamines

myxedema

caused by extreme deficiency of thyroid secretion; also known as adult hypothyroidism -severe manifestation -crisis state; decreased metabolism to other tissues -accumulation of fluid interrupts airway!

acromegaly

enlargement of the extremities. Hypersecretion of GH after long bones have developed. -Adult manifestation

How are steroid hormones formed?

formed on demand from cholesterol that is stored in the cell or retrieved from the circulating lipoproteins

cyclic hormone regulation

hormone is regulated so that it increases in the blood at a constant time and roughly the same amount -ex. rising or falling after sleep

Cell signaling (autocrine)

hormone molecule secreted by a cell affects the secreting cell

Cell signaling (paracrine)

hormone molecule secreted by one cell affects adjacent cells

Gluconeogenesis

making glucose from non-carb substances (Formation!)

Cell signaling (endocrine)

secretion of hormones into the bloodstream by endocrine glands -Most endocrine hormones are polypeptides manufactured on the rough endoplasmic reticulum and stored in vesicles within the cells.

Cell signaling (neurocrine)

secretion of hormones into the bloodstream by neurons