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Pathophysiology of Obesity: A Comprehensive Overview, Study notes of Human Physiology

Reva University Human Physiology

A comprehensive overview of the pathophysiology of obesity, exploring its genetic, environmental, hormonal, inflammatory, and systemic components. It delves into the definition and classification of obesity, the role of energy balance and adipose tissue dynamics, and the metabolic dysregulation associated with the condition. The document also discusses the systemic and mechanical effects of obesity, as well as its psychological and neurological impacts. It concludes by highlighting the importance of a multidisciplinary approach to managing and preventing obesity.

Typology: Study notes

2024/2025

Available from 02/21/2025

tanushree-maharana 🇮🇳

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Pathophysiology of Obesity

Obesity is a multifactorial chronic disease characterized by excessive fat accumulation that

adversely affects health. It is associated with an increased risk of numerous comorbidities,

including metabolic syndrome, cardiovascular diseases, type 2 diabetes, and certain cancers. A

thorough understanding of the pathophysiology of obesity involves exploring its genetic,

environmental, hormonal, inflammatory, and systemic components.

1. Definition and Classification

 Definition: Obesity is a condition defined by excessive body fat accumulation. It is

typically assessed using the Body Mass Index (BMI), calculated as weight in kilograms

divided by the square of height in meters (kg/m²).

o Normal BMI: 18.5–24.9 kg/m².

o Overweight: 25–29.9 kg/m².

o Obesity: ≥30 kg/m².

 Classification by Fat Distribution:

o Visceral (Android) Obesity: Fat accumulation in the abdominal region, closely

linked with metabolic complications, including insulin resistance, dyslipidemia,

and cardiovascular diseases.

o Subcutaneous (Gynecoid) Obesity: Fat deposition in the hips and thighs,

associated with fewer metabolic risks.

 Other Measures:

o Waist-to-Hip Ratio: High ratios indicate increased visceral fat.

o Waist Circumference: A strong predictor of obesity-related metabolic disorders.

2. Etiology of Obesity

Genetic Factors:

 Monogenic Obesity: Rare mutations in leptin, leptin receptor, and melanocortin-4 receptor

(MC4R) genes disrupt hypothalamic regulation of appetite and energy expenditure.

 Polygenic Obesity: Over 300 loci have been identified through genome-wide association

studies (GWAS). Variants in the FTO gene are strongly associated with increased adiposity.

 Epigenetic Regulation: Environmental factors can modify gene expressio n through

mechanisms like DNA methylation, influencing obesity risk across generations.

Environmental and Lifestyle Factors:

 Dietary Habits: Consumpt ion of energy-dense, high-fat, and highly processed foods

promotes obesity.

 Physical Inactivity: Reduced physical activity levels due to sedentary lifestyles contribute

to a positive energy balance.

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Pathophysiology of Obesity Obesity is a multifactorial chronic disease characterized by excessive fat accumulation that adversely affects health. It is associated with an increased risk of numerous comorbidities, including metabolic syndrome, cardiovascular diseases, type 2 diabetes, and certain cancers. A thorough understanding of the pathophysiology of obesity involves exploring its genetic, environmental, hormonal, inflammatory, and systemic components.

1. Definition and Classification  Definition: Obesity is a condition defined by excessive body fat accumulation. It is typically assessed using the Body Mass Index (BMI), calculated as weight in kilograms divided by the square of height in meters (kg/m²). o Normal BMI: 18.5–24.9 kg/m². o Overweight: 25 – 29.9 kg/m². o Obesity: ≥30 kg/m².  Classification by Fat Distribution: o Visceral (Android) Obesity: Fat accumulation in the abdominal region, closely linked with metabolic complications, including insulin resistance, dyslipidemia, and cardiovascular diseases. o Subcutaneous (Gynecoid) Obesity: Fat deposition in the hips and thighs, associated with fewer metabolic risks.  Other Measures: o Waist-to-Hip Ratio: High ratios indicate increased visceral fat. o Waist Circumference: A strong predictor of obesity-related metabolic disorders. 2. Etiology of Obesity Genetic Factors:  Monogenic Obesity: Rare mutations in leptin, leptin receptor, and melanocortin-4 receptor (MC4R) genes disrupt hypothalamic regulation of appetite and energy expenditure.  Polygenic Obesity: Over 300 loci have been identified through genome-wide association studies (GWAS). Variants in the FTO gene are strongly associated with increased adiposity.  Epigenetic Regulation: Environmental factors can modify gene expression through mechanisms like DNA methylation, influencing obesity risk across generations. Environmental and Lifestyle Factors:  Dietary Habits: Consumption of energy-dense, high-fat, and highly processed foods promotes obesity.  Physical Inactivity: Reduced physical activity levels due to sedentary lifestyles contribute to a positive energy balance.

 Sleep Deprivation: Alters hormonal regulation of hunger (ghrelin) and satiety (leptin), promoting overeating.  Medications: Corticosteroids, antipsychotics, and some antidepressants contribute to weight gain. Socioeconomic and Cultural Influences:  Access to high-calorie foods, urbanization, and socioeconomic status are significant determinants of obesity prevalence.

3. Dysregulation of Energy Balance Energy Intake and Expenditure:  Positive Energy Balance: Excess caloric intake relative to expenditure leads to fat storage in adipose tissue.  Role of Hypothalamus: The hypothalamus integrates hormonal signals (e.g., leptin, ghrelin, and insulin) to regulate appetite, energy expenditure, and thermogenesis. Leptin Resistance:  Leptin, secreted by adipocytes, signals satiety to the hypothalamus. In obesity, high circulating leptin levels fail to suppress appetite due to central resistance, perpetuating weight gain. Role of Ghrelin:  Ghrelin, secreted by the stomach, stimulates hunger. Its levels rise before meals and fall after eating. Dysregulation of ghrelin contributes to hyperphagia in obesity. 4. Adipose Tissue Dynamics

6. Metabolic Dysregulation Insulin Resistance and Hyperinsulinemia:  Elevated free fatty acids and cytokines interfere with insulin receptor signaling, impairing glucose uptake and promoting hyperglycemia. Lipotoxicity:  Excess lipids accumulate in non-adipose tissues (e.g., liver, muscle, pancreas), causing cellular dysfunction and conditions like non-alcoholic fatty liver disease (NAFLD). Dyslipidemia:  Obesity-related dyslipidemia involves elevated triglycerides, increased low-density lipoprotein (LDL), and decreased high-density lipoprotein (HDL). 7. Systemic and Mechanical Effects Cardiovascular Complications:  Hypertension, dyslipidemia, and atherosclerosis are prevalent in obesity due to chronic sympathetic activation and systemic inflammation. Mechanical Burden:  Obstructive Sleep Apnea (OSA): Excess pharyngeal tissue narrows airways during sleep.  Osteoarthritis: Increased weight accelerates joint degeneration.  Gastroesophageal Reflux Disease (GERD): Elevated intra-abdominal pressure promotes reflux and esophageal damage. 8. Psychological and Neurological Effects  Mood Disorders: Obesity is associated with depression, anxiety, and low self-esteem.  Neurological Impacts: Chronic inflammation may contribute to neurodegenerative diseases like Alzheimer's. 9. Other Contributing Factors Microbiome Dysbiosis:  Gut microbiota influence energy harvest from food and regulate inflammation. Obesity alters microbial composition, promoting weight gain. Hormonal Disruptions:  Cortisol, thyroid hormones, and sex hormones affect fat distribution and metabolic health. Sympathetic Nervous System (SNS):  Chronic overactivity in obesity contributes to hypertension and metabolic dysfunction. 10. Conclusion

Obesity is a complex condition arising from a combination of genetic, environmental, and physiological factors. Its pathophysiology involves dysregulated energy balance, chronic inflammation, insulin resistance, and systemic metabolic disturbances. Beyond metabolic derangements, obesity imposes mechanical and psychological burdens, significantly reducing quality of life. Addressing the pathophysiology of obesity requires a multidisciplinary approach, including lifestyle modification, pharmacotherapy, and, in severe cases, surgical intervention. Effective management and prevention strategies are critical in mitigating its global health burden.