Reproductive Cyclicity

Hi :) In this post we'll discuss reproductive cyclicity. I'll describe the stages of the oestrus cycle and differentiate it from the menstrual cycle. We'll take a look at the three forms of anoestrus as well as monoestrus and polyoestrus animals. We'll also discuss the role of melatonin in seasonal breeders and differentiate between the reproductive cycles of the bitch, queen, ewe and mare. Finally we'll explain how the use of teasers and artificial lighting can be used to manipulate oestrus cycles. 

Oestrus vs Menstrual Cycles

There are two types of reproductive cyclicity in animals: oestrus cycles, which occur in non-primates, and menstrual cycles, which occur in primates. During an oestrus cycle, the body reabsorbs the endometrium if conception fails and a bloody discharge comes from blood vessels. There is also a significant behaviour change in these animals during oestrus and animals are only receptive to mating during 'heat'. An oestrus cycle lasts approximately 20 days and may continue until death. 

Menstrual cycles includes bleeding which results from the endometrium being shed if conception fails. These animals are theoretically receptive to mating throughout the cycle which lasts approximately 28 days. Menstruation ceases at menopause.  

Phases of the Oestrus Cycle

This cycle can be divided into two major stages which both include two stages:

• Follicular Phase: this includes:
• Proestrus: this involves the formation of ovulatory follicles and oestradiol secretion. It begins after the corpus lutea are destroyed and follicle stimulating hormone (FSH) and lutenising hormone (LH) are prominent. This lasts for about 2-5 days.
• Oestrus: the animal becomes sexually receptive and oestrus behaviour is demonstrated. Peak oestradiol secretion occurs. Ovulation occurs once oestrogen levels reach a threshold level.
• Luteal Phase, which includes:
• Metoestrus: after ovulation, one or more corpus lutea (CL) develop in the ovaries and progesterone secretion begins. This also lasts for about 2-5 days
• Dioestrus: A mature CL secretes large amounts of progesterone which prompts the uterus to prepare for embryo development. This stage terminates when the CL is destroyed. It is the longest stage and lasts for 10-14 days in polyoestrus animals.

 Variations in Cyclicity

Anoestrus refers to when a female does not exhibit regular oestrus cycles, the ovaries and inactive and both ovulatory follicles and CL are absent. Anoestrus is caused by insufficient gonadotropin releasing hormone (GnRH) secretion and there are three forms:

• True anoestrus: this is caused by insufficient nutrition, lactation or stress.
• Apparent anoestrus: this is a result of the failure to detect oestrus or pregnancy.
• Seasonal anoestrus: this is normal in animals who are seasonal breeders. 

Oestrus cycles are categorised according to how frequently they occur throughout the year:

• Monoestrus: these are animals with only one oestrus cycle per year. Dogs are an example of an animal with this type of cycle, although they may display 1-2 cycles per year. 
• Continually Polyoestrus: this is when oestrus cycles occur regularly throughout the entire year and pregnancy can occur regardless of season. Cattle, cats and pigs demonstrate this type of cycle.
• Seasonally Polyoestrus (short-day breeders): these animals display clusters of oestrus cycles in a particular season and they begin to cycle as the day length decreases (autumn/winter). Sheep and goats demonstrate this. 
• Seasonally Polyoestrus (long-day breeders): These animals display clusters of oestrus cycles in a season and they begin to cycle as day length increases (spring). Horses display this type of cycle.

Differences in Reproductive Cycles Between Species

  Canine

A domestic female displays 1-2 oestrus cycles per year. This consists of a proestrus and oestrus lasting 9 days each, dioestrus lasting 2 months and anoestrus lasting 5 months. Ovulation occurs during oestrus three days after the LH surge. The female is receptive to the male while estradiol is decreasing and progesterone in the body is increasing to coincide with ovulation.

Feline

The feline oestrus cycle consists of proestrus, oestrus, postoestrus, dioestrus and anoestrus. They are induced ovulators which means they require copulation in order to ovulate. Postoestrus occurs between oestrus periods in cats that have not ovulated. The female enters oestrus, which lasts for 9 days, every 17 days. 

Sheep: 

Melatonin secretion from the pineal gland occurs during hours of darkness and translates the changes in photoperiod into neural impulses. Melatonin is progonadotropic in the ewe as it causes GnRH to be secreted which results in the secretion of LH and FSH. In sheep, the first ovulation following anoestrus is 'silent' and no behavioural changes occur. In order for behavioural oestrus to happen progesterone needs to be present for a period of time before oestrogen is secreted. Progesterone acts as a primer to increase the brain's sensitivity to oestrogen.

Horses

In horses, melatonin is antigonadotropic as it inhibits the secretion of GnRH and hence the secretion of LH and FSH. In these animals, anoestrus is caused by melatonin which is secreted in response to increasing darkness (winter). During spring time, melatonin secretion is decreased and this allows GnRH to be released which leads to LH and FSH secretion. The transition between anoestrus and oestrus periods is called the vernal transition and results in overt sexual or oestrus behaviour. 

Teasers and Artificial Lighting

 Pheromones provide information on the sexual or social status of the emitter and are released in bodily fluids or produced and kept on the emitter's body. Female reproductive cycles in animals can be stimulated and synchronised by introducing a male teaser. A teaser is a surgically prepared male used to sexually tease but not impregnate females. They can be vasectomised males or castrates that have been injected with testosterone.

Day length can also be adjusted in order to manage fertility, particularly in seasonally polyoestrus animals. With horses, artificial lighting can be used to shift the vernal period earlier in the year. This increases the number of breedings possible in a season. 


That's it for this post, see you next time :)



 

Hormonal Aspects of the Male Reproductive System

Hello :) This post will deal with the hormonal aspects of the male reproductive system. I'll describe the basic anatomy and function of the testes with particular emphasis on the sertoli and leydig cells. I'll also describe the hypothalamic-pituitary-testicular hormonal axis and the role of hormones involved in spermatogenesis. We'll take a look at the negative feedback system used by the body to regulate the male reproductive system as well as the synthesis and effects of testosterone within the male body. We'll also discuss the role of adrostenone in pigs as well as the factors that affect male fertility. I'll finish off by explaining cryptorchidism.

Anatomy and Function

The testes have two main functions: spermatogenesis, the formation of male gametes, and testosterone synthesis, the principal male sex hormone. Ninety per cent of testicular mass consists of seminiferous tubules which are the site of spermatogenesis. Seminiferous tubules consist of:

1. Sertoli cells: these are located in the walls of the seminiferous tubules and are the site of spermatozoa formation (spermatogenesis). They also synthesise inhibin under the influence of Follicle Stimulating Hormone (FSH).
2. Leydig Cells: these are interspersed in the interstitial region of the testis between seminiferous tubules. They are responsible for testosterone synthesis in response to lutenising hormone (LH). LH binds to these cells and this stimulates the synthesis of testosterone from cholesterol. Testosterone is secreted within 30 minutes of an LH surge. LH is released in bursts and this is critical because it prevents the desensitisation of Leydig cells to LH which may occur if exposed for long periods of time. In addition, if testosterone where present in the blood constantly, negative feedback would prevent LH and FSH release.

 Testosterone Synthesis

The process of testosterone synthesis is summarised in the flow diagram below:

Cholesterol

↓

                                StAR - Rate Limiting Step

↓

Pregnenolone

↓

Progesterone

↓

17 OH-progesterone

↓

Androstenedione

↓

Testosterone

↓

       Blood       OR      Sertoli Cells
                                ↓

                              Converted to Estradiol or DHT

 
In this process, StAR transfers the cholesterol to the inner mitochondrial membrane and is the rate-limiting step. Testoseterone is then produced which can either diffuse into the blood or, more commonly, into sertoli cells where it is converted to estradiol or dihydrotestosterone (DHT). DHT is the more active form of testosterone in the body.

Testosterone isn't very soluble in blood and so most of it travels bound to several substances. Forty-five per cent is bound to sex-hormone binding globulin (SHBG), 50% to albumin and roughly 0.5% is free and bioavailable. Testosterone and DHT bind to intracellular receptors, complex to DNA in the nucleus and increase gene transcription. In many tissues, such as the prostate and penis, DHT is more important than testosterone. However, in skeletal muscle and bones, testosterone is the most important.

Actions of Testosterone

Testosterone has several actions on the body, including:

• Anabolic Actions: enhances skeletal muscle and bone growth and stimulates protein synthesis while inhibiting its breakdown.
• Reproductive Actions: Testosterone is responsible for the differentiation of the male internal and external genitalia in the foetus. It is also involved in the growth, development and function of the male internal and external genitalia as well as the initiation and maintenance of spermatogenesis.
• Secondary Sex Characteristics: These are characteristics which distinguish between males and females but are not part of the reproductive system. Testosterone is responsible for:
• increasing sex drive
• territorial marking
• development of antlers, horns and tusk-like teeth
• pheromones: these are odorous molecules secreted in the saliva, urine or feces.
• development of combs and unique plumage. 

 Hypothalamic-Pituitary-Testicular Hormonal Axis

The hormonal regulation of reproduction is primarily controlled by the interaction between the hypothalamus, anterior pituitary and testes. The hypothalamus secretes gonadotropin releasing hormone (GnRH) which stimulates the anterior pituitary to release FSH and LH. These hormones affect the testes by causing germ cell development, as well as the secretion of androgens, oestrogens and progesterone. 

GnRH is released in a pulsatile manner and its secretion is influenced by a variety of internal and external signals including: stress, temperature, nutrition, light, social cues and steroid hormones. 

Both males and females produce FSH and LH. FSH primarily stimulates gametogenesis as well as the secretion of inhibin which has a negative effect on FSH. LH stimulates secretion of androgens from the testes as well as oestrogens and progesterone in the ovaries. It is essential for final follicle maturation and ovulation. FSH and LH are known as gonadotropic hormones because they stimulate the growth and development of the gonads.

Regulation of the Male Reproductive System

Steroid hormones are the most important regulator of the male reproductive system. Steroid hormones provide negative feedback at the pituitary and hypothalamus as they slow the release of GnRH at the hypothalamus and reduce the sensitivity of the pituitary to GnRH, lowering the secretion of LH and FSH. Inhibin, synthesised by the sertoli cells, suppresses the release of FSH only. 


Androstenone in Pigs

This substance is an androgen which is produced in the testes along with testosterone in pigs. It has a characteristic smell and acts as a sex pheromone in saliva by eliciting a copulatory stance in sows that are in oestrus. Androstenone is also responsible for 'boar taint' which makes boar meat difficult to market. For this reason, male pigs which are intended for market are often castrated.

Factors which Affect Male Fertility

Several factors affect male fertility in animals, this includes:

• Daylength: Daylength determines the breeding season in seasonal breeders. Daylength can be altered in order to adjust breeding seasons by using indoor lighting (this is often done in the poultry industry).
• Nutrition: Nutrition and feeding practise has a large effect on the fertility of an animal.
• Stress: this is usually associated with deleterious effects on reproduction. Stresses include social stressors, environmental stressors, transport, nutritional/metabolic stressors, disease/infection, and predation stressors. 
• Social Cues: Pheromones provide information on the sexual or social status of the emitter and males use the scent of females to asses whether they are in oestrus or not. 

Cryptorchidism

Cryptorchidism is a condition in which one or both testes has failed to descend into the scrotum during development. It is common in stallions and boars and is the most common disorder of sexual development in dogs. It is important that cryptorchids are always desexed because the condition is inherited and tumours commonly develop within cryptorchid testes, these often turn cancerous. 
 

That's all for this post, if you have any questions please feel free to ask : )


 
 

Pineal Gland

Hi :) In this physiology post we'll investigate the differences in pineal gland function between the lower and higher vertebrates. I'll also describe the pathway for light detection and the subsequent release or synthesis of melatonin and explain the importance of this substance in maintaining circadian rhythm. I'll finish off by explaining how melatonin regulates many aspects of reproduction including the variation in species breeding seasons.

Pineal Gland Function

The pineal gland secretes melatonin, a potent antioxidant which controls the sleep/wake cycle, and is highly innervated by the sympathetic nervous system. It consists of primordial photoreceptive cells and retains light sensitivity in lower vertebrates (such as fish). However, in higher vertebrates it has evolved as a secretory organ. It has no photoreceptivity but responds to light-encoded information which is relayed to the pineal gland.

Pathway of Light to the Pineal Gland:

This pathway is summarised in the flow diagram below:

Light reaches retinal photoreceptors

                                                    ↓ via the retinohypothalamic tract

Suprachiasmatic Nucleus

↓

Sympathetic nerve fibres extend from the superior
cervical ganglion to the pineal gland

↓

Norepinephrine binds to β-adrenergic receptors on pinealocytes

↓

cAMP promotes AANAT synthesis

↓

NAT converts serotonin to melatonin in the hours of darkness.

Melatonin is not stored and instead is released immediately following synthesis. Synthesis is regulated by the enzyme AANAT (this stands for arylalkylamine N-acetyltransferase. We don't need to remember this though!). Reduced light causes the release of norepinephrine from sympathetic nerve terminals in the pinealocytes and this results in increased AANAT synthesis and therefore increased melatonin synthesis and release. 

Melatonin synthesis must be highly regulated to maintain circadian rhythms. A circadian rhythm is any self-sustaining biological process that oscillates approximately every 24 hours. The body determines day length based on the duration of melatonin secretion at night (and not the concentration of melatonin in the body). 

Melatonin and Reproduction

Melatonin influences GnRH secretion (Follicle stimulating hormone and lutenising hormone). Thus the length of daylight can influence gonadotropin secretion, reproductive cycles, gonad size as well as the timing and onset of puberty.

Seasonal Breeders

With these animals, reproduction is timed so that offspring are born at an optimal time of year when food and resources are abundant (spring). Photoperiod alters melatonin secretion by the pineal gland which regulates the release of gondotropin releasing hormone (GnRH) from the hypothalamus. This alters FSH and LH secretion from the anterior pituitary.

Melatonin signals the duration of photoperiod and the interpretation of this by the central nervous system will vary with species. In short-day breeders (sheep and goats) melatonin is progonadotropic while in long-day breeders (horses, rodents, and birds) it is antigonadotropic.

Melatonin may also affect reproduction in males by influencing testis diameter, particularly in short-day breeders. 

That's all for this post, if you have any questions please feel free to ask :)

Parathyroid

Parathyroid Gland

Hi, in this post we’ll be taking a look at the parathyroid gland which plays an important part in the regulation of calcium (Ca) and phosphorus (P) balance within the body. We’ll take a look at where calcium, phosphorus and magnesium are stored in the body as well as the role of the kidneys, digestive tract, bone and skin in maintaining calcium balance. In addition, we’ll discuss the anatomical structure of the parathyroid as well as the major physiological actions of parathyroid hormone (PTH). We’ll discuss the factors which affect the secretion of PTH and calcitriol and the process by which calcitriol is synthesised. We’ll also talk about calcium sensing receptors and a few disorders that are involved with calcium regulation.

Structure of the Parathyroid

Four parathyroid glands are found in mammals and they consist primarily of chief cells. In dogs and cats two external glands are present outside the thyroid and two internal glands are present inside the thyroid. The cells of the parathyroid are arranged into dense cords or nests around abundant capillaries. This provides the products of these cells easy access to the bloodstream.

 

Location of Storage Sites

Ninety-nine per cent of all Ca2+ in the body is found in bone in the form of hydroxyapatite crystals. Some Ca is also found in the extracellular fluid (the interstitial fluid and blood plasma) as ionized Ca (iCa, which is biologically active), complexed with other ions, and bound to proteins. Intracellularly, Ca is found mainly in the mitochondria and sarcoplasmic reticulum.

Eighty-five per cent of total P is stored in bone in the form of hydroxyapatite. Phosphorus is also found in the extracellular fluid as inorganic phosphates as well as in the intracellular fluid in its organic form (eg. Enzyme, phospholipids, ATP etc.).

The majority of magnesium is stored in bone, muscle and other soft tissue while less that 1% is present in the extracellular fluid and plasma.  

Calcium Balance

Kidneys, Digestive Tract, Bone and Skin

The plasma calcium concentrations are regulated by the kidneys, digestive tract, bone and skin. Calcium is added to the plasma by absorption from the digestive tract, resorption (mobilisation) of bone and reabsorption of calcium at the kidneys. Calcium can be removed from the plasma by calcification of bone and filtration at the kidneys.

PTH, Calcitriol and Calcitonin

In addition to the body systems described above, three hormones regulate calcium balance. These are parathyroid hormone (PTH), calcitriol (also called 1, 25-(OH)₂D₃), and calcitonin. The most important regulator of calcium and phosphorus in the extracellular fluid and blood is PTH.

PTH increases plasma calcium levels by:

• Stimulating the resorption of bone. Osteoblasts (which are responsible for laying down new bone) have surface proteins (RANKL) which bind to a receptor (RANK) on osteoclasts (responsible for breaking down bone) causing them to be activated. Osteoblasts prevent the activation of osteoclasts by secreting OPG which blocks this binding. PTH increases the synthesis of RANKL and decreases the amount of OPG, this leads to increased osteoclast activation which causes bone to be resorbed.
• Stimulating calcium reabsorption in the ascending loop of Henle and distal tubules of the kidneys. PTH also inhibits the reabsorption of phosphate in the proximal and distal tubules and this helps to maintain the correct Ca:P ratio during hypocalcaemia. 
•  Stimulating the activation of calcitriol in the kidneys. It does this by increasing the hydroxylation (and activation) of 1, 25-(OH)₂D₃ in the proximal tubule. This promotes the absorption of calcium in the GIT, reabsorption of calcium at the kidneys as well as bone resorption.

Calcitonin lowers plasma levels of calcium and phosphorus by impairing osteoclast-mediated bone resorption and by decreasing renal reabsorption of C and P. Calcitonin secretion is directly determined by the levels of Ca in the blood, high Ca = high calcitonin.

Regulation of PTH and Calcitriol

The major regulator of PTH secretion is the concentration of iCa in the plasma. A drop in iCa in plasma stimulates PTH release and this is mediated by Calcium-Sensing receptors (CaSR). Although a rise in serum Ca decreases PTH secretion it will never halt PTH secretion completely. Thus the body is better equipped to deal with hypocalcaemia than hypercalcaemia because PTH levels can be increased to deal with low calcium more than they can be decreased to deal with excess calcium. Factors other than Ca concentrations can also affect the secretion of PTH, this includes:

1.       1,25(OH)₂D₃: Calcitriol supresses gene transcription which reduces PTH synthesis but this is overridden by hypocalcaemia.

2.       Phosphate: High P concentrations stimulate the secretion of PTH. This is because it directly lowers plasma iCa²⁺ through the formation of calcium phosphate

3.       Magnesium: Hypermagnesemia reduces PTH secretion.

Calcitriol

A vitamin D precursor, 7-dehydrocholesterol is converted to vitamin D3 in the presence of sunlight and is released into plasma. Vitamin D3 can also be absorbed from the diet. Vitamin D3 then undergoes the unregulated conversion to 25(OH)D₃ in the liver which is then released into the plasma. This substance then undergoes the regulated conversion to 1,25(OH₂)₃D_3, in the proximal convoluted tubule of the kidney and is also released into the plasma. This is regulated by calcium and PTH plasma concentrations. A low calcium concentration causes more PTH to be released which stimulates this conversion. This causes the reabsorption of Ca in the kidneys and gastrointestinal tract and leads to an increase in plasma Calcium concentrations.

Disorders of Calcium Regulation

Hypocalcaemia

Hypocalcaemia may be a result of decreased bone resorption, as well as reduced GIT and renal absorption of calcium. The body attempts to maintain near-normal serum calcium and phosphate levels, this results in:

•   High PTH and 1,25-(OH₂)D₃ 
•  Increased bone resorption leading to osteopenia (termed osteoporosis in humans) 
•  Increased intestinal absorption of Ca 
•  Decreased fractional excretion of Ca in the kidney 
• Increased fractional excretion of P in the kidney.

Milk Fever in Dairy Cows

This is a metabolic disorder of dairy cows which occurs close to the time of calving. This is due to the extremely high calcium requirements of the developing calf and early lactation. Thus, feed management during the two weeks before calving is critical in order to prevent this condition.

Milk Fever causes agitation, excitement and muscle tremors in the animal. This then causes the animal to stagger and take up a ‘sitting’ position, after which the cow may lie flat on its side. This unfortunately may lead to circulatory collapse, coma and death.

Hypocalcaemia in Small Animals

Hypocalcaemic tetany (eclampsia) is common in small dog breeds which become pregnant with large litters. It occurs between 1-3 weeks after pregnancy due to the loss of calcium during lactation or poor diet. It results in seizures, trembling and stiffness in the animal.

Renal failure is also a common cause of hypocalcaemia in dogs as failure causes an inability to synthesise 1,25(OH₂)D₃.

Nutritional Secondary Hyperparathyroidism

This condition is associated with a diet which is low in calcium and/or high in phosphate and results in increased PTH secretion which leads to osteopenia of long bones and vertebrae. It is most common in young, growing animals particularly in large and giant breeds.

That’s all from me for this post, see you next time :)

Growth Hormone

Hello :) In this post we'll explore the regulation of growth hormone (GH) secretion, the association between GH and somatomedins (IGFs) and their effects on body growth and metabolism. We'll also take a look a the major abnormalities associated with abnormal GH secretion. Finally, I'll explain why growth hormone has been used in production animals and describe the importance of ghrelin in GH secretion. Enjoy!

Effects on Growth and Metabolism

GH is a peptide hormone which is synthesised by the somatotrope cells in the anterior pituitary and has several effects on the body.

Growth - Indirect Anabolic Effects:

The indirect growth effects of GH are mediated by somatomedins (insulin-like growth factors). GH stimulates the liver to produce IGFs which act as "classical hormones", while others IGFs produced in other parts of the body work locally as paracrines. IGFs are very important and mediate cell growth and proliferation in most cells but its major target is bone and muscle. 

GH causes new bone to be laid by osteoblasts on the outer surface while bone is resorbed by osteoclasts on the inner circumference of bones. This causes the bone circumference to increase with a simultaneous increase in the diameter of the marrow cavity while the weight of the bone remains the same. GH also causes the addition of new bone at the epiphyseal plates of bones. In this process, new cartilage is deposited and then is converted to new bone.

GH also causes an increased cellular uptake of amino acids for protein synthesis as well as a decreased rate of protein breakdown from muscle. It also causes increased cell size (hypertrophy) and proliferation (hyperplasia). 

Metabolism - Direct Catabolic Effects

GH acts an antagonist to insulin and causes a decrease in the uptake of glucose by adipose and muscle cells. It also causes an increase in glucose production by the liver through gluconeogenesis (see this post). Overall it is diabetogenic, that is it increases plasma glucose concentrations.

Growth Hormone also has an effect on lipids by activating hormone sensitive lipase resulting in an increase in lipolysis (see this post). This causes increased fat metabolism and a decrease in fat deposition and the use of fats as energy in order to conserve glucose is encouraged. Overall, GH causes an increased concentration of plasma fatty acid concentrations.   

Regulation

The secretion of GH is under dual regulation by the hypothalamus:

1. GH Releasing Hormone (GHRH): this binds to the GHRH receptor and stimulates GH synthesis and secretion. The release of GHRH is pulsatile, thus GH release is also pulsatile. 
2. Somatostatin (SS) or Growth Hormone Inhibiting Hormone (GHIH): this is a potent inhibitor of GH release but has no effect on synthesis. The secretion of SS increases with a rise in GH or IGF-1 (insulin-like growth factor 1)

GH follows a daily cycle as well as lifetime secretory patterns. Daily, secretion follows circadian rhythms where there is increased secretion at night, peaking at early morning. The pulsatile secretion is due to the pulsatile release of GHRH from the hypothalamus. Over the course of an animal's life, there is an increased release of GH as a neonate and at puberty while secretion decreases with older age.   

 IGF-1 is a major determinant of negative feedback control as an increase in insulin-like growth factor secretion results in a decrease in GHRH secretion and an increase in SS secretion. In addition, hypoglycaemia, decreased plasma fatty acids and amino acids will result in an increase in GH secretion. Stress, circadian rhythms, sleep and ghrelin also causes an increase in GH secretion. 

Ghrelin

Ghrelin is secreted mainly by the stomach and is the hormone of hunger as its concentration increases before meals and decreases afterwards. Ghrelin binds to the GH secretagogue receptor (GHSR) and this induces the synthesis and secretion of GH from the pituitary.  

Abnormalities

Pituitary Dwarfism 

This is a congenital deficiency of GH (which leads to low IGF-1 levels which cause the ineffective growth of bones and muscles). Clinical signs include short stature, bone deformities and well as a variety of endocrine related coat and skin problems. It seems that German Shepherd dogs are predisposed to this condition. 

Gigantism:

This isn't reported in animals but does occur in humans. It occurs because of an excess secretion of GH before the epiphyseal plates close and results in an abnormally large stature, but in proportion. Associated problems include cardiac hypertrophy, glucose intolerance, hyperinsulinaemia, and premature death. 

Acromegaly:

This causes enlarged extremities because excessive GH secretion occurs after the epiphyseal plates close. This results in the growth of soft tissue and an increase in bone circumference. This condition is mostly seen in cats due to chronic pituitary neoplasia (the abnormal proliferation of cells) which causes:

• increased size of the head, feet and abdomen
• organ hypertrophy
• diabetogenic effects
• insulin-resistant diabetes mellitus. 

The Use of Growth Hormones in Production Animals 

Growth hormones are species specific and pharmacologic administration of GH leads to:

• increased feed efficiency
• improved muscle mass
• reduced carcass lipid content
• increased carcass protein content
• increased milk production (by up to 10-40%)

That's all for this post, if you have any questions please feel free to ask in the comments section below :)

Chemical Properties of Soils

Hi :) In this post we'll be discussing the chemical properties of soils. I'll explain cation exchange capacity, why it is important and how it changes with soil type. We'll discuss the cause and effects of soil acidity as well as the causes of salinity. In addition, we'll take a look at the nitrogen and phosphorus cycles.

Cation Exchange Capacity

Cations are positively charged ions which are attached to the edge of clay particles or organic matter by electrostatic forces. Clay particles are flat crystals that are made up of many thin sheets which are held together by hydrogen or water. This creates a large surface area which allows more cations to attach to the clay particles which are negatively charged. The total capacity of a soil to hold exchangeable cations is known as the Cation Exchange Capacity (CEC).

CEC is important because it influences the ability of the soil to retain essential nutrients and acts as a buffer against acidification. In addition, most of the exchangeable cations are needed by plants and animals. This includes ions such as calcium, magnesium, sodium and potassium ions as well as hydrogen, aluminium, and manganese ions as the soil becomes more acidic. The level of these ions and the balance between them may lead to imbalances, deficiencies or toxicities.

Soils with high clay proportions tend to have a higher CEC while sandy soils rely on the high CEC of organic matter to retain nutrients in their top soil. CEC varies according to:

• The amount of clay present
• The type of clay: smectites are the best clay type because they have the highest CEC.
• Soil pH
• The amount of organic matter present.

 Soil Acidity

Soil acidification is a natural process which has been accelerated by agriculture. Acidification has two main causes:

1. Inefficient use of Nitrogen: Nitrogen in the form of ammonia (NH4) is readily converted to nitrate(NO3 -) and hydrogen (H+) in the soil. If nitrate is not used by plants it may leach away, this results in an accumulation of H+ which ultimately reduces the pH.
2. Removal of plant material: Most plant material is slightly alkaline and the removal of this material by grazing or harvest leaves excess hydrogen ions in the soil. Over time, as this process is repeated, it leads to a decrease in pH.

 Soil acidity has several effects on the soil:

• When soil pH drops, aluminium becomes more soluble. In its soluble form, aluminium retards root growth and restricts access to water and nutrients.  
• Low pH also leads to decreased availability of nitrogen, phosphorus, potassium, sulphur, calcium, manganese and molybdenum. 
• A decreased pH also lowers microbial activity, especially the nitrogen fixing rhizobia. 

Acidic soils can be improved by the addition of lime which increases the soil's pH. 

Salinity

Salts are carried inland from the ocean by wind and rainfall and they have been accumulating in clay sub-soils for long periods of time. Before European settlement in Australia, native vegetation used up most of the rainfall. This kept the water table low and the salt remained deep in the soil profile.

When the Europeans arrived, the widespread clearing of vegetation and the use of shallow-rooted annual plants, which use less water than native vegetation, resulted in rising water tables. Salt rises with the water tables and evaporation leaves the salt at the surface. Rising salinity reduces soil productivity and kills vegetation.
 
Phosphorus

Phosphorus is essential for plant and animal growth and is one of the most critical and limiting nutrients in agriculture. Unfortunately, it is almost universally deficient in Australian soils in their natural state and this results in stunted plant growth.

Phosphorus fertiliser is added to soils in a water soluble form. This then reacts in the soil to form insoluble and more stable compounds which are inaccessible to plants. There is competition between the soil and plants for access to phosphorus as only 5-30% of the phosphorus applied will actually be used by crops.

Nitrogen

Nitrogen is needed by plants in larger quantities than any other nutrient. Most nitrogen in soils is present in an organic form, that is it's associated with organic matter, plant residues, organisms, and animal waste. Organic nitrogen is mineralised to inorganic forms such as nitrate and ammonia by microbes and this occurs slowly over the growing season providing a steady supply of nitrogen to the plants. For this course we only need a general understanding of the nitrogen cycle. This website provides an excellent explanation of the topic.


That's all for this post, if you have any questions please feel free to ask :)
 
 

Adrenal Glands

Hello :) In this post we'll be learning about the adrenal glands. We'll discuss the anatomical structure of the adrenal gland as well as the actions of the hormones that this gland produces. We'll also take a detailed look at the synthesis of glucocorticoid hormones and explain the regulatory mechanisms which control the synthesis and secretion of adrenocorticoid and catecholamine hormones. We'll also discuss hypo- and hyperadrenocorticism and list the different types of adrenergic receptors and the response they bring about following activation. Enjoy!

Structure 

The adrenals are paired glands located at the superior poles of the two kidneys and are composed of an outer cortex (80%) and inner medulla (20%).

The cortex is composed of three different histological layers:

• zona glomerulosa (thinnest and outer most): this secretes mineralocorticoids (eg. aldosterone)
• zona fasciculata (middle and thickest): secretes glucocorticoids (eg. cortisol) and a smaller quantity of sex hormones.
• zona reticularis (inner most): secretes sex hormones (androgens which are converted to oestrogens) and a smaller quantity of glucocorticoids

Each of these layers produces different hormones. 

Adrenocorticoids

Hormone Synthesis:

The Adrenal Cortex hormones (adrenocorticoids) share a common mechanism of synthesis. Steroid hormones all come from a cholesterol precursor. Low density lipoproteins (LDLs) (see this post) are responsible for 80% of the cholesterol delivered to the adrenal glands. The LDL-receptor complex is endocytosed and digested by lysosomes. It is then transferred to the inner mitochondrial membrane by steroidogenic acute regulatory (StAR) proteins. The substance is then converted to pregnenolone by the cytochrome P450scc (side chain cleavage) enzyme. Pregnenolone then enters the endoplasmic reticulum and undergoes multiple complex steps to be converted to mineralocorticoids, glucocorticoids or androgens. The rate limiting step of this whole process is the movement of cholesterol into the mitochondria by the StAR protein. 

Glucocorticoids

Actions:

Glucocorticoids have a range of actions which help to maintain homeostasis. They work by binding to specific glucocorticoid receptors in the cell nucleus and this alters gene expression. Basically, their function is to mobilise body fuels, particularly during times of stress and their effects are catabolic. In terms of carbohydrate metabolism, they increase gluconeogenesis and glycogenolysis and enhance the actions of glucagon. This increases blood glucose concentration. In addition, these hormones inhibit glucose uptake and utilization by peripheral tissues. This slows down the consumption of blood glucose.

 In terms of protein metabolism, the hormones stimulate protein catabolism and inhibit protein synthesis, however, the brain and cardiac muscle is protected. 

In terms of fat metabolism, they enhance lipolysis and this causes free fatty acids to be released into the blood stream. Plasma cholesterol concentrations also increase and fat deposits are redistributed. 

Glucocorticoids also induce negative calcium balance through inhibition of intestinal absorption and increased renal excretion. They also inhibit osteoblast function and this may result in osteoporosis.

These hormones also diminish the inflammatory and immune response. 

Mineralocorticoids (Aldosterone):

Action

Aldosterone binds to receptors in the cytosol of the principal cells of the late distal tubule and collecting ducts of the kidney. The binding of this hormone stimulates the synthesis and opening of sodium and potassium ion channels on the apical membrane. On the basolateral membrane it causes the synthesis and insertion of Na/K pumps. These two actions simultaneously increase sodium reabsorption and potassium secretion.

Catecholamines

Action

Catecholamines include adrenaline and noradrenaline (also called epinephrine and norepinephrine, respectively). These hormones are used as neurotransmitters by the sympathetic division of the autonomic nervous system. These substances bind to adrenergic receptors which are present in most cells of the body. There are four subtypes of adrenergic receptors and each responds differently to the catecholamines:

• ·α1 : these are located on the postsynaptic nerve endings. They cause vascular smooth muscle contraction which results in vasoconstriction and increased blood pressure.

• ·     α 2: these are found on pre- and post-synaptic nerve endings. They inhibit noradrenaline, have mixed effects on smooth muscle and cause vasodilation.

• ·          β1: these are found in the heart. They have positive inotropic (cause an increase in the force of contraction) and chronotropic (increase heart rate) cardiac effects. They also increase renin secretion and adipocyte lipolysis.

• ·          β2: Found in skeletal muscle, arterioles and bronchioles. They cause smooth muscle vasodilation, bronchodilation and uterine relaxation.

 

Regulation of Synthesis and Secretion of Catecholamines and Adrenocorticoids

Adrenocorticotropic Hormone (ACTH) primarily stimulates the synthesis of glucocorticoids and androgens. In the short term it causes a StAR mediated increase in cholesterol delivery to the mitochondria. In the long term it stimulates the synthesis of steroidogenic enzymes. The secretion of ACTH is controlled by corticotropin-releasing hormone (CRH) which is released by the anterior pituitary gland (See this post).  

Disorders of the Adrenal Glands

Hypoadrenocorticism:

This is also known as Addison’s disease in dogs and is characterised by significantly reduced cortisol and aldosterone levels. There are three types of hypoadrenocorticism:

·         Primary: this may be idiopathic (spontaneous), immune mediated or drug induced destruction of the adrenocortical tissue.

·         Secondary: due to impaired hypothalamic-pituitary function

·         Iatrogenic: this is when normal secretion may be impaired following the withdrawal of glucocorticoid therapy. This is because it takes time for the adrenal cortex to start producing its own hormones again.

Clinical signs include: hyponatraemia/hyperkalaemia, hypovolaemia and dehydration, vomiting or diarrhoea, and hypothermia.

Hyperadrenocorticism:

This is also known as Cushing’s Syndrome in dogs and results in the excess secretion of hormones from the adrenal cortex. There are three forms of this syndrome:

• Pituitary Dependent (80%): Excessive ACTH secretion by the pituitary (most commonly because of a tumour) results in bilateral adrenal hyperplasia which causes excess cortisol secretion and the failure of the negative feedback system of ACTH. 
• Adrenal dependent 
• Iatrogenic

Clinical signs include: muscle wasting and weakness as a result of increased protein catabolism and decreased protein synthesis; secondary infection due to a compromised immune system; abdominal distention due to the redistribution of fat deposits and polyphagia causing weight gain; alopecia because hair growth is inhibited; as well as panting and respiratory changes because of exercise intolerance and muscle wasting from protein catabolism.

That's it for this post, if you have any questions please feel free to ask :)