The document summarizes various hormones and signaling molecules secreted by adipose tissue, known as adipokines. It discusses leptin, adiponectin, resistin, visfatin, and omentin, describing their production in adipose tissue, mechanisms of regulation, receptor interactions, functions, and implications for metabolic health conditions like obesity and type 2 diabetes. The adipokines influence processes like appetite regulation, insulin sensitivity, inflammation, and vascular function. Ongoing research aims to better understand their roles in metabolic disease pathogenesis and potential as therapeutic targets.

1. EHSAN AHMAD MLT
MEDICAL LABORATORY SCIENTIST AT SUPERIOR UNIVERSITY
LAHORE
PRESENTATION ON
ENDOCRINE SECRETIONS OF ADIPOSE TISSUE

2. CONTENT LIST
• 1.Asipose tissue
• 2. Leptin Hormone
• 3.Adiponectin
• 4.Resistin
• 5.Viafatin
• 6.Omentin

3. ADIPOSE TISSUE
• Adipose tissue also known as fat tissue is of two types
• White adipose tissue (stores e energy)
• Brown adipose tissue (provide body heat)
• Adipose tissue is considered an endocrine organ because it produces
and releases hormones. Adipocytes (fat cells) secrete various hormones
and signaling molecules, collectively referred to as adipokines. Leptin
and adiponectin are examples of adipokines that play roles in appetite
regulation and metabolic processes, highlighting the endocrine
functions of adipose tissue.

4. LEPTIN
• 1. Production:-Source.
• Mainly synthesized and secreted by white adipose tissue.
• Other Sources
• Also produced by other tissues like brown adipose tissue, placenta, ovaries,
skeletal muscle, stomach, and mammary epithelial cells.
• 2. Regulation
• Fat Mass Sensitivity:
• Leptin production is directly proportional to fat mass. More adipose tissue leads to
higher leptin levels.
• Circadian Rhythm:
• Secretion follows a circadian rhythm, with levels peaking during the night.
• 3. Receptor Interaction:
• Leptin Receptor:
• Acts by binding to the leptin receptor (ObR), primarily located in the
hypothalamus.

5. • Transport Across the Blood-Brain Barrier:
• Leptin must cross the blood-brain barrier to exert its effects on the central nervous system.
• 4. Signaling Pathways:
• JAK-STAT Pathway:
• Binding of leptin to its receptor activates the JAK-STAT (Janus kinase-signal transducer and activator of
transcription) pathway, influencing gene expression. -
• PI3K-Akt Pathway:
• * Involved in the regulation of energy balance and metabolism.
• 5. Functions:
• Appetite Regulation:
• Leptin acts as a crucial regulator of appetite and energy balance by signaling satiety to the brain, especially
the hypothalamus. - *
• Energy Expenditure:
• Influences energy expenditure and thermogenesis in brown adipose tissue.
• Reproductive Function:
• Plays a role in reproductive physiology by influencing the hypothalamic-pituitary-gonadal axis.

6. • Immune Modulation:
• Impacts immune function and inflammation regulation.
• 6. Clinical Implications:
• Leptin Resistance:
• In conditions of obesity, individuals may develop leptin resistance, where despite high levels of
leptin, its signaling is impaired.
• Dysregulation in Eating Disorders:
• Anorexia nervosa is associated with low leptin levels, reflecting a state of energy deprivation.
• 7. Impact on Diseases:
• Obesity:
• Leptin is often elevated in obesity, but its effectiveness in regulating appetite may be diminished
due to leptin resistance.
• Type 2 Diabetes:
• Leptin resistance may contribute to the development of insulin resistance seen in type 2 diabetes.
• Leptin stands as a key player in the intricate network regulating energy homeostasis, and its
dysregulation has profound implications for metabolic health, making it a significant focus of
research in the fields of obesity, diabetes, and eating disorders.

7. ADIPONECTIN
• 1. Production and Sources:
• Origin:
• Adiponectin is predominantly synthesized by adipocytes,
with higher levels found in subcutaneous fat.
• Release:
• It is released into the bloodstream, with factors like adipose
tissue mass influencing its secretion dynamics.
• 2. Regulation Mechanisms:
• Adiposity Influence:
• Adiponectin levels inversely correlate with adiposity. This
is regulated by mechanisms involving transcriptional
control and post-translational modifications.

8. • 3.Adiponectin Receptors and Signaling
Pathways:
• Receptor Interaction:
• Adiponectin binds to AdipoR1 and AdipoR2, initiating intracellular signaling.
• Downstream Pathways:
• Activation of AMP-activated protein kinase (AMPK) and peroxisome
proliferator-activated receptor-alpha (PPAR-α) pathways contributes to its
metabolic effects
• 4. Multifaceted Functions:
• Insulin Sensitivity:
• Adiponectin enhances insulin sensitivity by promoting glucose uptake and
inhibiting hepatic gluconeogenesis.
• Anti-Inflammatory Properties:
• It exerts anti-inflammatory effects by suppressing pro-inflammatory cytokines
and modulating immune responses.
• Vascular Protection:
• Adiponectin improves endothelial function, inhibits vascular inflammation,
and protects against atherosclerosis.

9. • 5.Clinical Implications and Disease Associations:
• Insulin Resistance and Type 2 Diabetes:
• Low adiponectin levels are associated with insulin resistance and type 2 diabetes. Modulating adiponectin levels may hold therapeutic potential.
• Cardiovascular Diseases:
• Adiponectin deficiency is linked to cardiovascular diseases, suggesting a role in maintaining cardiovascular health.
• Adiponectin emerges as a crucial adipokine with diverse functions, influencing metabolic, inflammatory, and vascular processes.
• Its intricate regulation and multifaceted roles make it a subject of ongoing research, holding promise for therapeutic interventions in metabolic and cardiovascular diseases.

10. RESISTIN
• 1.Production and Sources:
• Primary Origin:
• Resistin is mainly secreted by adipocytes, particularly those in white adipose tissue.
• Extracellular Release:
• After production, Resistin is released into the bloodstream, contributing to its endocrine
function
• 2.Regulation Mechanisms:
• Influence of Inflammation:
• Resistin expression is influenced by inflammatory signals, and its release is often
upregulated in states of inflammation.
• Insulin Resistance Link:
• Resistin is associated with insulin resistance, and its levels may be elevated in conditions
where insulin sensitivity is impaired.

11. • 3. Receptor Interaction and Signaling:
• Receptor Target:
• Resistin binds to receptors, including adenylyl cyclase-
associated protein 1 (CAP1) and Toll-like receptor 4 (TLR4).
• Downstream Signaling:
• Activation of these receptors can trigger intracellular pathways
involved in inflammation and insulin resistance.
• 4. Functions:
• Insulin Resistance:
• Resistin has been implicated in the development of insulin
resistance, affecting insulin sensitivity in peripheral tissues like
skeletal muscle and liver.
• Pro-Inflammatory Effects:
• Resistin promotes inflammation by influencing immune cell
function and releasing pro-inflammatory cytokines.

12. • 5. Clinical Implications and Disease Associations:
• Metabolic Disorders:
• Elevated Resistin levels are often observed in conditions associated with metabolic dysfunction, such as obesity and type 2 diabetes
• Cardiovascular Impact:
• Resistin may contribute to cardiovascular diseases through its pro-inflammatory effects and influence on endothelial function.
• Resistin, while still a subject of ongoing research, emerges as a hormone with potential implications in metabolic health.
• Its connections to insulin resistance and inflammation position it as a key player in understanding the intricate interplay between adipose tissue and systemic metabolic regulation.

13. VISFATIN
• 1.Production and Sources:
• Adipose Tissue Origin:
• Visfatin, also known as Nicotinamide Phosphoribosyltransferase (Nampt), is primarily produced and secreted by adipocytes, particularly visceral
adipose tissue.
• Extracellular Release:
• Once synthesized, visfatin is released into the bloodstream, contributing to its endocrine function.
• 2. Regulation Mechanisms:
• Metabolic Factors:
• Expression of visfatin can be influenced by metabolic factors, and its release may be modulated in response to changes in nutritional status.
• Inflammation Link:
• Visfatin expression may be upregulated in states of inflammation.

14. • 3. Receptor Interaction and Signaling:
• Receptor Target:
• Visfatin binds to the insulin receptor, albeit with lower affinity than insulin.
• NAMPT Activity:
• As an enzyme, Nampt in the extracellular space catalyzes the conversion of nicotinamide to nicotinamide mononucleotide (NMN), a key step in
the salvage pathway for NAD+ biosynthesis.
• 4. Functions:
• Insulin-Mimetic Effects:
• Visfatin exhibits insulin-mimetic effects by activating insulin receptor signaling pathways, contributing to glucose uptake in certain tissues.
• NAD+ Biosynthesis:
• The conversion of nicotinamide to NMN by visfatin plays a role in maintaining NAD+ levels, influencing cellular metabolism and energy
balance.
• Inflammatory Modulation:
• Visfatin may have anti-inflammatory effects, and its regulation in inflammatory conditions suggests a potential role in immune responses.

15. • 5. Clinical Implications and Disease Associations:
• Insulin Sensitivity:
• Visfatin's insulin-mimetic effects raise questions about its potential implications in insulin sensitivity
and glucose homeostasis.
• Metabolic Disorders:
• Altered visfatin levels have been observed in metabolic disorders, including obesity and type 2
diabetes, prompting investigations into its role in these conditions.
• Inflammatory Conditions:
• Visfatin's association with inflammation suggests possible involvement in inflammatory diseases.
• Visfatin, with its dual roles as a hormone and an enzyme involved in NAD+ biosynthesis, presents a
fascinating area of study in the complex network of adipose tissue hormones and their systemic
effects.
• Ongoing research aims to uncover the full spectrum of visfatin's functions and its potential therapeutic
applications.

16. OMENTIN
• 1. Production and Sources:
• Distinct Forms:
• Omentin exists in two primary forms - Omentin-1 and Omentin-2.
• Adipose Tissue Origin:
• Both forms of omentin are produced by visceral adipose tissue, distinguishing them as adipokines.
• 2. Regulation Mechanisms:
• Metabolic Factors:
• Omentin levels may be influenced by metabolic factors, with research exploring the regulation of its expression
in response to changes in nutritional status.
• Inflammatory Conditions:
• The expression of omentin, particularly Omentin-1, may be modulated in states of inflammation.

17. • 3. Receptor Interaction and Signaling:
• Receptor Binding:
• The specific receptors through which omentin exerts its effects are still under investigation.
• Downstream Signaling:
• Research is ongoing to understand the intracellular pathways activated by omentin upon binding to its receptors.
• 4. Functions:
• Insulin Sensitivity:
• Omentin-1 is particularly associated with enhancing insulin sensitivity in peripheral tissues like skeletal muscle and adipose tissue.
• Anti-Inflammatory Properties:
• Omentin, especially Omentin-1, displays anti-inflammatory effects, influencing immune responses and reducing pro-inflammatory cytokine
production.
• Vascular Protection:
• Omentin is implicated in vascular health, with potential effects on endothelial function and protection against atherosclerosis.

18. • 5. Clinical Implications and Disease Associations:
• Insulin Sensitivity and Diabetes:
• Omentin levels have been found to be altered in conditions associated with insulin resistance, including type 2 diabetes.
• Cardiovascular Health:
• Reduced levels of omentin, particularly Omentin-1, are observed in cardiovascular diseases, suggesting a potential role in maintaining vascular
health.