Endo: Final Written Response

Obesity: central integration of energy homeostasis
What is that? Give an example.
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Obesity: central integration of energy homeostasis
What is that? Give an example.
Signals (adapting food intake to energy expenditure:

How does Leptin signal the brain?
1. Presence of adipose tissue (fat) = presence of Leptin

2. LepR receives signals from Leptin

3. NPY/AGRP (agouti-related peptide) and POMC (pro-opiomelanocortin) neurons in the arcuate nucleus of the hypothalamus send projections to second order neurons (alpha-MSH and AGRP) in other regions of the hypothalamus (PVN)

4. both alpha-MSH and AGRP act on a common receptor, the melanocortin-4 receptor (MC4R) expressed on PVN neurons

5. The MC4R neurons then innervate (excite) neurons in other areas of the hypothalamus and brain stem to produce an integrated inhibition of appetite and increase in energy expenditure

Possible causes for obesity:
> OMIM deficiency (leptin receptor deficiency)
- BBB level causing impermeability
- disregulated hypothalamic cells that fail to respond to leptin once it crosses over and stop feeding behavior
- leptin is one of the central mediators of energy homeostasis

> mutation of MC4R

> mutation of POMC

> changes in insulin
Adrenal Gland: Fig. 9-8; hypothalamic-pituitary axis in adrenal insufficiency
- understand the figure focus on adrenal insufficiency
HPA in adrenal deficiency of different causes

Normal state:
hypothalamus secretes CRH
->
pituitary secretes ACTH
->
adrenal cortex secretes cortisol (negative feedback loop inhibits more secretion of CRH and ACTH) and aldosterone

Primary adrenal insufficiency (PAI or Addison's disease):
- issue in the adrenal cortex means no cortisol is secreted
- no negative feedback loop
- CRH and ACTH levels remain high

Secondary adrenal insufficiency ACTH deficiency):
- issue in the pituitary means ACTH is not produced
- high CRH; low ACTH and low cortisol

Tertiary adrenal insufficiency (CRH deficiency):
- issue with the hypothalamus
- CRH is not secreted
- low CRH; low ATCH; low cortisol
Hormone: parathyroid hormone-related protein (PTHrP).
Syndrome:
hypercalcemia
Hormone: parathyroid hormone (PTH)
Syndrome:
hypercalcemia
Hormone: adrenocorticotropin (ACTH)
Syndrome:
cushings syndrome (specifically disease)
Hormone: corticotropin-releasing hormone (CRH)
Syndrome:
cushing syndrome
Hormone: antidiuretic hormone (ADH)
Syndrome:
hyponatremia (low blood sodium level)
Hormone: insulin and insulin-like growth factors
Syndrome:
hypoglycemia
Hormone: growth hormone-releasing hormone (GHRH)
Syndrome:
acromegaly
Hormone: human chorionic gonadotropiin (hCG)
Syndorme:
children - precocious puberty
men - erectile dysfunction
women - dysfunctional uterine bleeding
Hormone: fibroblast growth factor (FGF) 23Syndrome: oncogenic osteomalaciaHormone: vasoactive intestinal peptide (VIP)Syndrome: diarrheaEndocrine tumors: Table 21-1; describe one syndrome in detail - dont need to include treatments - give details as much as possible - cell types, feedback loops, etc.- tumor in anterior pituitary gland (hyperplasia) can lead to over secretion of ACTH (from corticotroph cells) - leading to increase in cortisol levels from adrenal cortex (zona fasciculata) - for example, in Cushing's disease - most common cause of tumor is an adenoma - adenoma = a benign noncancerous tumor - controls the body's use of carbs, fats, and proteins, reduces immune system response to swelling (inflammation) and regulates blood pressure and body's water balanceSex hormones: Describe folliculogenesis or spermatogenesis; Fig 12-1 (for spermatogenesis describe the 3 phases)Spermatogenesis: - process by which male gametes are developed - when rounded immature sperm cells undergo successive mitotic and meiotic divisions (spermatocytogenesis) and a metamorphic change (spermiogenesis) to produce spermatozoa - hormones in process include: GnRH, LH, FSH, and testosterone GnRH: acts on anterior pituitary gland and stimulates the release of LH and FSH LH: stimulates interstitial/Leydig cells to secrete androgens (testosterone) FSH: acts directly on spermatogonia to produce sperms and on Sertoli cells to concentrate androgens via membrane-bound receptor - determines # of Sertoli cells ABP (androgen binding protein): secreted by Sertoli cells - required to bind and concentrate testosterone in the seminiferous tubules - spermatogenesis is controlled Bia negative feedback loop in the HPT axis STAR protein: controls transport of cholesterol from the outer to the inner mitochondrial membrane