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Obesity

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The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in adipocytes...

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An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes

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From obesity to diabetes.

¹University Hospital Basel, CH-4031 Basel, Switzerland. ukeller@uhbs.ch

International Journal for Vitamin and Nutrition Research. Internationale Zeitschrift Fur Vitamin- Und Ernahrungsforschung. Journal International De Vitaminologie Et De Nutrition

|January 24, 2007

Summary

Obesity significantly increases the risk of insulin resistance and type 2 diabetes by affecting adipocyte function and increasing free fatty acids. Lifestyle changes, including weight loss and increased physical activity, are crucial for preventing diabetes development.

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

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Published on: January 7, 2018

Area of Science:

Metabolic disorders and endocrinology
Obesity and diabetes research
Cardiovascular risk factors

Background:

Rising global obesity rates are linked to increased insulin resistance and type 2 diabetes.
Obesity, particularly visceral obesity, is a key component of the metabolic syndrome, characterized by insulin resistance, hypertension, and dyslipidemia.
Adipocytes contribute to insulin resistance through free fatty acid release and secretion of inflammatory cytokines like TNF-alpha and interleukin-6.

Purpose of the Study:

To review the pathogenetic mechanisms linking obesity and type 2 diabetes.
To highlight the role of adipocytes and associated molecular factors in insulin resistance.
To discuss the therapeutic potential of PPAR-gamma agonists and the importance of lifestyle interventions.

Main Methods:

Review of scientific literature on obesity, insulin resistance, and type 2 diabetes.
Analysis of the molecular and cellular mechanisms involved in metabolic dysfunction.
Examination of clinical trial data on lifestyle interventions and pharmacological treatments.

Main Results:

Excess adipocytes impair insulin sensitivity and contribute to the metabolic syndrome.
Adipocytes secrete factors (adiponectin, resistin, TNF-alpha, IL-6) that promote insulin resistance.
Increased free fatty acids negatively impact glucose metabolism and pancreatic beta-cells.
Visceral adipose tissue enhances cortisol metabolism, contributing to insulin resistance.
Thiazolidinediones (glitazones) improve insulin sensitivity by targeting PPAR-gamma.
Lifestyle modifications (weight loss, physical activity, diet) significantly inhibit progression from prediabetes to type 2 diabetes.

Conclusions:

Obesity is a primary driver of insulin resistance and type 2 diabetes through complex pathogenetic mechanisms.
Targeting adipocyte dysfunction and metabolic pathways offers therapeutic strategies.
Lifestyle interventions, including weight management and physical activity, are fundamental for diabetes prevention.