Carbohydrate metabolism and stress: the role of glucagon and insulin
Stress and prolonged physical exertion require the immediate mobilization of energy resources. This task is performed by glucagon, a hormone of the $\alpha$-cells of the islets of Langerhans in the pancreas, which acts as the main antagonist of insulin.
Glucagon secretion is stimulated by hypoglycemia, stress, physical activity, as well as under the influence of the sympathetic nervous system and growth hormone (via somatomedin). Its production is suppressed by insulin, somatostatin, and high glucose levels.
Physiological effects of glucagon:
- Carbohydrate metabolism: causes a pronounced hyperglycemic effect. It activates glycogen phosphorylase (stimulating glycogenolysis) and inhibits glycogen synthase (slowing its formation). Additionally, gluconeogenesis is stimulated.
- Fat metabolism: exerts a lipolytic and ketogenic effect. Triglyceride levels decrease, and ketone bodies appear in the blood.
- Conclusion: tissues receive the glucose and ketone bodies necessary to overcome stress.
The regulation of insulin secretion is also subject to changes: parasympathetic influences stimulate it, whereas sympathetic influences and the paracrine action of somatostatin (from $\delta$-cells) inhibit it. Somatostatin acts by activating the inhibitory G-protein cAMP system, suppressing the secretion of many cells, including insulin and glucagon.
Adaptation to circadian rhythms: pineal gland and melatonin
The pineal gland is a gland of neuroglial origin that synthesizes biogenic amines (serotonin, norepinephrine, histamine) and peptide hormones. The main factor in adaptation to changing lighting conditions is melatonin.
Melatonin synthesis directly depends on illumination: signals are perceived by the retina and transmitted reflexively via the sympathetic nervous system. In the light, the conversion of serotonin to melatonin is inhibited, while in the dark, it increases sharply. This cyclic production determines daily (circadian) biological rhythms.
Effects of melatonin:
- Sleep regulation: an increase in hormone levels causes a sedative effect, facilitating the transition from wakefulness to sleep.
- Metabolic suppression: inhibits the secretion of hormones that increase metabolism (ACTH, TSH, GH).
- Influence on reproduction: determines the cyclicity of gonadotropic effects (including the duration of the ovarian-menstrual cycle).
Adaptation of mineral metabolism: parathyroid glands
Two pairs of parathyroid glands, located posteriorly or within the thyroid gland, secrete parathyroid hormone (PTH). Its sole purpose is to maintain normal blood calcium levels through a strict negative feedback mechanism: a decrease in calcium stimulates PTH production, while an increase inhibits it.
Mechanisms of PTH action:
- In bone tissue: activates osteoclasts, causing bone demineralization and the release of calcium into the blood.
- In the kidneys: enhances calcium reabsorption, decreases phosphate reabsorption (increasing their excretion), and stimulates the synthesis of calcitriol, the active form of vitamin D.
Hemodynamic adaptation: the endocrine role of the kidneys and RAAS
Although the kidneys do not have specialized glands, their cells produce many biologically active substances: calcitriol, erythropoietin, thrombopoietin, prostaglandins, and kallikrein. Of particular importance is renin, an enzyme of the juxtaglomerular apparatus that triggers the renin-angiotensin-aldosterone system (RAAS).
Factors activating renin secretion:
- A decrease in blood pressure in the afferent arteriole.
- An increase in the concentration of $Na^+$ ions in the urine of the distal tubule (detected by cells of the macula densa — macula densa).
- Sympathetic influences (via $\beta$-adrenoceptors) and adrenaline.
Note: atrial natriuretic peptide and high pressure suppress renin secretion.
The RAAS cascade and its effects:
- Renin converts plasma-circulating angiotensinogen (synthesized in the liver) into the weakly active angiotensin I.
- Angiotensin-converting enzyme (ACE, predominantly from the lungs) converts it into active angiotensin II.
Angiotensin II causes powerful vasoconstriction, activates the sympathetic nervous system, induces the sensation of thirst, and prompts the zona glomerulosa of the adrenal cortex to secrete aldosterone. Aldosterone, in turn, increases the reabsorption of $Na^+$, $Cl^-$, and $HCO_3^-$ in the kidneys, leading to water retention in the body. The system is regulated by negative feedback depending on the levels of $Na^+$, $K^+$, angiotensin, and aldosterone in the blood.
RAAS cascade: Renin Releases Angiotensinogen → ACE Activates Angiotensin II → Aldosterone Accumulates sodium and water.
Class and exam questions
How does the body regulate melatonin production?
Stress activates the sympathetic nervous system, which stimulates the release of glucagon. Glucagon activates glycogen phosphorylase, breaking down glycogen, and stimulates gluconeogenesis, leading to the release of glucose into the blood.
What serves as a signal for melatonin production?
The main signal is a change in illumination. Information from the retina is transmitted via the sympathetic nervous system to the pineal gland: in the dark, synthesis from serotonin increases, while in the light, it is inhibited.
What is the role of macula densa cells in adaptation to pressure changes?
The cells of the macula densa act as sodium receptors. When sodium concentration in the distal tubule urine increases, they signal to enhance renin secretion.
Where else, besides the kidneys, can renin be produced?
Extrarenal production of renin occurs in the vascular walls of other organs, in the brain, and in the salivary glands.
What else to study on this topic
- Paracrine effects of somatostatin via G-proteins
- Mechanisms of sodium reception in the macula densa
- Extrarenal renin synthesis: role in local blood flow
- The connection between the sympathetic nervous system and glucagon production
- The role of atrial natriuretic factor as a RAAS antagonist
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