Fisiología Endocrina - Hormona de Crecimiento (GH) e IGF-1 (IG:@doctor.paiva)

Name: Fisiología Endocrina - Hormona de Crecimiento (GH) e IGF-1 (IG:@doctor.paiva)
Uploaded: 2021-03-06T00:16:37.000Z
Duration: 1 h 20 min 9 s

Introduction

The instructor introduces the topic of growth hormone and insulin-like growth factor 1 (IGF-1).

General Information about Growth Hormone and IGF-1

Growth hormone (GH) and IGF-1 are hormones involved in growth and development.

GH is released by somatotropes in the anterior pituitary gland.

GH release is regulated by the hypothalamus through the release of GH-releasing hormone (GHRH) and somatostatin.

IGF-1 is produced mainly in the liver and is stimulated by GH.

Hypothalamus-Pituitary Axis

The instructor explains the relationship between the hypothalamus and pituitary gland in regulating GH secretion.

Hypothalamus-Pituitary Communication

The hypothalamus releases GHRH to stimulate somatotropes to produce and release GH.

Somatostatin, also released by the hypothalamus, inhibits GH production and secretion.

Types of Pituitary Cells

The instructor describes different types of cells in the pituitary gland that produce various hormones.

Types of Pituitary Cells

Somatotropes synthesize and release GH.

Other cell types include lactotropes (prolactin), corticotropes (adrenocorticotropic hormone), thyrotropes (thyroid-stimulating hormone), gonadotropes (luteinizing hormone, follicle-stimulating hormone).

Functions of Growth Hormone

The instructor discusses the main functions of GH.

Functions of Growth Hormone

GH promotes growth in tissues, both through hypertrophy (increase in cell size) and hyperplasia (increase in cell number).

It has anabolic effects on various tissues.

GH also plays a role in metabolism, including lipolysis and glucose regulation.

Actions of Growth Hormone

The instructor explains the direct and indirect actions of GH.

Direct and Indirect Actions of Growth Hormone

GH directly stimulates cell growth and division.

Indirectly, GH stimulates the liver to produce IGF-1, which mediates many of the growth-promoting effects of GH.

Effects on Bone and Muscle

The instructor discusses the effects of GH on bone and muscle tissue.

Effects on Bone and Muscle

GH promotes both bone hypertrophy (increased size) and hyperplasia (increased cell number).

It also stimulates muscle growth by increasing protein synthesis.

Insulin-like Growth Factor 1 (IGF-1)

The instructor introduces IGF-1 as a mediator of GH's effects.

Insulin-like Growth Factor 1 (IGF-1)

IGF-1 is a peptide hormone synthesized mainly in the liver.

It is responsible for mediating many of the indirect effects of GH on tissues.

IGF-1 promotes bone and tissue growth peripherally.

Conclusion

In this class, we learned about growth hormone (GH) and insulin-like growth factor 1 (IGF-1). GH is produced by somatotropes in the pituitary gland under the control of GHRH from the hypothalamus. GH has direct effects on cell growth and division, while IGF-1, produced in the liver, mediates many of the indirect effects of GH. GH promotes bone and muscle growth and plays a role in metabolism.

Actions of Growth Hormone (GH) and Insulin-like Growth Factor 1 (IGF-1)

This section discusses the actions of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) in various tissues.

GH Effects on Liver, Adipose Tissue, and Muscle

GH stimulates the liver to release IGF-1, which has multiple effects.

In adipose tissue, GH decreases glucose absorption and increases lipolysis.

In muscle tissue, GH decreases glucose absorption and increases amino acid uptake for protein synthesis.

GH Effects on Bones

GH has a direct effect on bones by increasing amino acid uptake and protein synthesis.

IGF-1 produced by the liver also enhances bone growth by increasing amino acid uptake and protein synthesis.

Negative Feedback Regulation of GH Release

IGF-1 inhibits the release of GH from both the hypothalamus and pituitary gland through negative feedback regulation.

Comprehensive Functions of GH

GH has direct effects on adipose tissue, liver, and muscle.

It decreases glucose absorption in adipose tissue and increases lipolysis.

It increases DNA synthesis, protein synthesis, and cell reproduction in the liver.

It promotes muscle growth by increasing amino acid uptake and protein synthesis.

Metabolic Effects of GH

Protein Deposition

GH promotes protein deposition in tissues by increasing protein synthesis in cells throughout the body. It facilitates amino acid transport across cell membranes, enhances energy utilization by transporters, and reduces protein degradation.

Fat Utilization

GH favors fat utilization as an energy source. It mobilizes fatty acids from adipose tissue into the bloodstream, leading to increased levels of free fatty acids. Excessive conversion of fatty acids into acetyl coenzyme A can cause ketoacidosis.

Carbohydrate Utilization

GH reduces the utilization of carbohydrates by tissues, favoring fat utilization instead.

Growth Effects of GH

Protein Synthesis

GH stimulates protein synthesis in various cells, leading to an increase in lean body mass. This effect is particularly desired by individuals aiming to build muscle mass.

Bone Growth

GH and IGF-1 promote bone growth by increasing amino acid uptake, protein synthesis, collagen production, and cell proliferation in chondrocytes.

Conclusion

GH and IGF-1 have diverse effects on different tissues. They play a crucial role in regulating metabolism, promoting protein deposition, utilizing fat as an energy source, and stimulating growth in bones and muscles. The negative feedback regulation ensures balanced hormone levels for maintaining homeostasis.

Effects of Insulin and Growth Hormone

This section discusses the effects of insulin and growth hormone on glucose metabolism and insulin resistance.

Insulin Resistance

Increased production of glucose in the liver leads to insulin resistance.

Growth hormone is a counter-insulin hormone that opposes the effects of insulin.

Growth hormone increases the production of free fatty acids, reducing sensitivity to insulin in the liver and skeletal muscles.

Synergistic Effects

Insulin and growth hormone have synergistic effects on certain processes.

Without insulin, growth hormone does not stimulate the production of IGF-1 (insulin-like growth factor 1).

Growth hormone has both counter-insulinic effects and synergistic effects on IGF-1 production.

Effects of Growth Hormone on Tissue Growth

This section explores the effects of growth hormone on tissue growth, particularly in bones.

Bone Growth

Growth hormone stimulates protein deposition and growth in various tissues.

The most prominent effect is seen in the skeleton, specifically in bone lengthening.

Growth hormone increases protein deposition in chondrocytes and osteogenic cells, promoting bone growth in length.

Differences between Lengthening and Thickening

Lengthening occurs through the deposition of new cartilage followed by its conversion into new bone until around age 25 when cartilage stops growing.

Thickening occurs through increased activity of osteoblasts, which synthesize more bone during adulthood.

Longitudinal vs. Thickness Growth

This section explains the differences between longitudinal (length) and thickness (girth) growth influenced by growth hormones.

Longitudinal Growth

Longitudinal or linear growth stops around age 25 when the growth plate (cartilage) disappears.

Growth hormone does not stimulate longitudinal growth after this age.

Thickness Growth

Thickness or girth growth continues throughout life.

Growth hormone, along with parathyroid hormone and estradiol, stimulates osteoblasts to produce more bone, resulting in increased thickness.

Gigantism vs. Acromegaly

This section discusses the differences between gigantism and acromegaly, two conditions caused by excess growth hormone.

Gigantism

Gigantism occurs when there is excessive release of growth hormones before the age of 25.

Individuals with gigantism experience linear growth due to stimulated bone development.

Acromegaly

Acromegaly occurs when there is excessive release of growth hormones after the age of 25.

Individuals with acromegaly do not experience linear growth but may have thicker bones, especially noticeable in facial features.

Puberty and Hormone Release

This section explains how puberty affects the release of growth hormones and their effects on bone growth.

Puberty and Maximum Growth Velocity

Puberty is a period of maximum growth velocity.

Growth hormone is released during puberty and has effects on IGF-1 production in both the liver and local bone receptors.

The transcript ends here.

New Section

This section discusses the relationship between growth and the plasma concentrations of IGF-1 during puberty. It also introduces the different receptors for growth hormone.

Receptors for Growth Hormone

The receptors for growth hormone (GH) are associated with tyrosine kinase.

There are two types of GH receptors: tyrosine kinase receptors and receptors associated with tyrosine kinase.

The liver has a receptor for GH, which stimulates the synthesis of insulin-like growth factor 1 (IGF-1).

New Section

This section explains the different mechanisms of action for the two types of GH receptors and their effects on hormone synthesis and secretion.

Mechanisms of Action

One type of GH receptor is associated with tyrosine kinase, while the other type is not.

The activation of protein kinases by GH leads to increased synthesis and secretion of GH.

Somatostatin, another hormone, inhibits protein kinases and thus inhibits GH synthesis and secretion.

New Section

This section explores the effects of GH on various organs and tissues, including adipose tissue, muscle, hepatocytes, cartilage, and bone.

Effects on Organs

GH has multiple effects on different organs.

In adipose tissue, muscle, and hepatocytes, it promotes gluconeogenesis and protein synthesis.

It also stimulates the release of IGF-1 from these tissues.

Additionally, GH indirectly affects visceral organs such as cartilage and bone through IGF-1.

New Section

This section discusses feedback regulation involving GH and its effects on the hypothalamus.

Feedback Regulation

GH binds to its carrier protein and inhibits the hypothalamus.

GH also has a short feedback loop, inhibiting its own secretion.

IGF-1, on the other hand, inhibits both the hypothalamus and the pituitary gland.

New Section

This section explores the factors that stimulate or inhibit GH release.

Stimuli for GH Release

Factors that stimulate GH release include hypoglycemia, exercise, fasting, stress, and deep sleep.

Testosterone and estrogen also stimulate GH release.

Inhibitors of GH Release

Factors that inhibit GH release include hyperglycemia, increased free fatty acids in the blood, aging, obesity, somatostatin, exogenous GH administration, and insulin-like growth factor 1 (IGF-1).

New Section

This section explains how GH is released from the hypothalamus to the pituitary gland and its effects on hormone production.

Release of GH

The hypothalamus releases growth hormone-releasing hormone (GHRH), which stimulates the production of GH in somatotropes.

Somatostatin released by the hypothalamus inhibits GH production.

New Section

This section describes how GHRH and somatostatin act on somatotropes in the pituitary gland.

Actions on Somatotropes

GHRH stimulates cAMP production in somatotropes through protein kinase activation.

Somatostatin inhibits cAMP production in somatotropes through protein kinase inhibition.

Overview of the Transcript

The speaker discusses the release and regulation of growth hormone (GH) in the body, focusing on the hypothalamus, pituitary gland, and various factors that influence GH secretion. They also touch upon the role of GH in different age groups and its effects on nutrition.

Regulation of Growth Hormone Release

The hypothalamus releases growth hormone-releasing hormone (GHRH), which stimulates the anterior pituitary gland to release GH.

Somatostatin, released by neurons in the peri-ventricular region of the hypothalamus, inhibits GH secretion.

Both GHRH and somatostatin travel through portal vessels to reach somatotroph cells in the anterior pituitary gland.

GH stimulates synthesis and release of GH by somatotroph cells, while somatostatin inhibits GH release.

Activation of protein kinase leads to an increase in intracellular calcium levels, causing exocytosis of pre-formed GH vesicles.

Factors Affecting Growth Hormone Secretion

In adults, GHRH from the hypothalamus stimulates GH release from somatotroph cells in the pituitary gland.

GF1 (insulin-like growth factor 1), produced by the liver under stimulation from GH, acts as a negative feedback mechanism to inhibit both adenohypophysis and hypothalamus.

GF1 can also inhibit its own production through negative feedback regulation.

The transport proteins for GH and GF1 differ in their binding affinity: GH has a shorter half-life due to weak binding with its transport protein compared to GF1's strong binding.

Normal Levels and Effects of Growth Hormone

Normal GH levels in adults range from 1.6 to 3 nanograms per milliliter, while children or adolescents have higher levels of around 6 nanograms per milliliter.

During prolonged fasting, GH levels can increase up to 50 nanograms per milliliter due to depletion of protein and carbohydrate reserves.

Acute hypoglycemia stimulates GH production more than protein deficiency, while chronic protein deficiency has a greater impact on GH secretion.

Severe malnutrition can significantly elevate GH levels, but treatment with carbohydrates alone does not reduce it as effectively as protein supplementation.

Effects of Nutrition on Growth Hormone

Adequate protein intake stimulates both GH and insulin release, leading to increased protein synthesis and growth without significant changes in calorie deposits.

A well-balanced diet with high protein intake promotes the release of GH and GF1, resulting in enhanced growth and development.

Summary: Growth Hormone Regulation and Effects

This section provides an overview of the regulation of growth hormone release by the hypothalamus and its effects on different age groups. It also discusses the influence of nutrition on growth hormone secretion.

Regulation of Growth Hormone Release

The hypothalamus releases GHRH to stimulate the anterior pituitary gland's somatotroph cells to secrete growth hormone (GH).

Somatostatin inhibits GH release from somatotroph cells.

Both GHRH and somatostatin travel through portal vessels to reach their target cells in the pituitary gland.

Factors Affecting Growth Hormone Secretion

In adults, GHRH stimulates GH release from somatotroph cells, while GF1 acts as a negative feedback mechanism to inhibit further GH secretion.

Transport proteins for GH and GF1 differ in their binding affinity, leading to differences in their half-lives.

Normal Levels and Effects of Growth Hormone

Normal GH levels range from 1.6 to 3 nanograms per milliliter in adults and around 6 nanograms per milliliter in children or adolescents.

Prolonged fasting can increase GH levels up to 50 nanograms per milliliter, while acute hypoglycemia stimulates GH production more than protein deficiency.

Severe malnutrition can significantly elevate GH levels, but protein supplementation is more effective than carbohydrate intake in reducing GH secretion.

Effects of Nutrition on Growth Hormone

Adequate protein intake stimulates both GH and insulin release, promoting growth and development without significant changes in calorie deposits.

New Section

The speaker discusses the effects of fasting on hormone production and protein synthesis.

Effects of Fasting

Fasting increases the production of growth hormone but decreases insulin levels. Insulin is necessary for the release of somatomedin or IGF1, which is important for protein synthesis.

In the absence of insulin during fasting, there will be a reduction in protein synthesis and growth. However, there will be an increased mobilization of calories from lipids.

It is important to understand that in the absence of insulin, the growth hormone does not stimulate the release of IGF1.

Please note that these notes are based on the provided transcript and may not capture all details from the video.