Periodontal innate immune mechanisms relevant to obesity.
Study Goal
The researchers aimed to explore the immunological consequences of obesity, particularly how a high-fat diet contributes to obesity and exacerbates infections like periodontal disease.
Results Summary
The study highlights that a high-fat diet contributes to obesity, which is linked to increased risk of infections such as periodontal disease, with Porphyromonas gingivalis as an example. It also notes that diet-induced obese (DIO) mouse models are more relevant for human obesity research than genetic models.
Population
General adult population, with focus on obese individuals (BMI > 30) and DIO mouse models.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
Obesity | increase | adult population of the USA | adult population of the USA | over 35% | affects | #1 |
Obesity-related illnesses | increase | leading cause of preventable death | worldwide population | - | emerged as | #2 |
Obesity | increase | cardiovascular disease | obese individuals | - | includes increased risk of | #3 |
Obesity | increase | type II diabetes | obese individuals | - | includes increased risk of | #4 |
Obesity | increase | cancer | obese individuals | - | includes increased risk of | #5 |
Obesity | increase | infections | obese individuals | - | includes increased occurrence and severity of | #6 |
Sedentary lifestyle and weight gain caused by consumption of a high-fat diet | increase | obesity | individuals | - | contribute to the development of | #7 |
Genetic models of obesity (ob/ob mice, db/db mice, and fa/fa rats) | no change | human obesity | human populations | - | have been insufficient to study | #8 |
Periodontal disease | increase | clinical variability and severity | general population | - | presents with | #9 |
Microorganism(s) associated with periodontal disease | increase | general population | general population | up to 46% | harbors | #10 |
Obesity | increase | periodontal disease | obese individuals | - | associated with increased incidence of | #11 |
Obesity | increase | immunological consequences | obese individuals | - | exacerbates effects of infection by pathogens | #12 |
Obesity affects over 35% of the adult population of the USA, and obesity-related illnesses have emerged as the leading cause of preventable death worldwide, according to the World Health Organization. Obesity's secondary morbidities include increased risk of cardiovascular disease, type II diabetes, and cancer, in addition to increased occurrence and severity of infections. Sedentary lifestyle and weight gain caused by consumption of a high-fat diet contribute to the development of obesity, with individuals having a body mass index (BMI) score > 30 being considered obese. Genetic models of obesity (ob/ob mice, db/db mice, and fa/fa rats) have been insufficient to study human obesity because of the overall lack of genetic causes for obesity in human populations. To date, the diet-induced obese (DIO) mouse model best serves research studies relevant to human health. Periodontal disease presents with a wide range of clinical variability and severity. Research in the past decade has shed substantial light on both the initiating infectious agents and host immunological responses in periodontal disease. Up to 46% of the general population harbors the microorganism(s) associated with periodontal disease, although many are able to limit the progression of periodontal disease or even clear the organism(s) if infected. In the last decade, several epidemiological studies have found an association between obesity and increased incidence of periodontal disease. This review focuses on exploring the immunological consequences of obesity that exacerbate effects of infection by pathogens, with focus on infection by the periodontal bacterium Porphyromonas gingivalis as a running example.