Dietary inflammatory index and its relation to the pathophysiological aspects of obesity: a narrative review

Abstract

Obesity, a complex disease that involves energy imbalance and chronic low-grade inflammation, is implicated in the pathogenesis of several chronic non-communicable diseases. As dietary components modulate the human body's inflammatory status, the Dietary Inflammatory Index (DII^®), a literature-derived dietary index, was developed in 2009 to characterize the inflammatory potential of a habitual diet. Abundant research has been conducted to investigate the associations between DII and obesity. In this narrative review, we examined the current state of the science regarding the relationships between DII and the inflammatory pathophysiological aspects related to obesity. DII is associated with inflammation in obesity. The most pro-inflammatory diet was directly related to higher levels of pro-inflammatory markers, which included C-reactive protein (CRP), interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α). Therefore, evidence suggests that the use of the DII may be useful for understanding the relationship between diet and the inflammatory process related to obesity.

Keywords: Inflammation; biomarkers; cytokines; diet; weight gain.

Figure 1. Obesity: etiological and pathophysiological aspects and the inflammation of adipose tissue and its effects. In obesity, there is a greater infiltration of immune cells in the adipose tissue, a change in phenotype from anti-inflammatory (M2) to pro-inflammatory (M1) macrophages, and dysregulated secretion of adipokines. Macrophages surround the adipocytes that have undergone pyroptosis and form crown-like structures (CLS), whose purpose is to remove debris from these adipocytes. Blue arrows indicate increased secretion (when pointed up) or decreased secretion (pointed down). Adapted from Calder el al. (48).

Figure 2. Relationship between the dietary inflammatory index, inflammation, and obesity. A negative dietary inflammatory index (anti-inflammatory DII) is associated with reduced inflammation and lower body weight, while a positive dietary inflammatory index (pro-inflammatory DII) is associated with increased inflammation and obesity. It is known that obesity increases blood inflammatory markers. However, some studies have shown a bidirectional action, where higher inflammatory markers could lead to obesity. a) Modulation of inflammation by food components through erythroid nuclear factor 2 related to factor 2 (Nrf2): Nrf2 is a transcription factor that is activated in response to oxidative stress and substances such as nitric oxide (NO), oxidized low-density lipoproteins (LDLox) and prostaglandins (PG). Nrf2, after activation, translocates to the nucleus, binds to Maf proteins (musculoaponeurotic fibrosarcoma) and to the antioxidant response element (ARE). In this way, it regulates genes that express enzymes with antioxidant and anti-inflammatory actions. Bioactive compounds can activate Nrf2, possibly by altering reactive cysteines within the Kelch-like ECH-associated protein 1 (Keap1), an adapter component of the Cul3 complex. As Nrf2 limits the levels of reactive oxygen species (ROS), food compounds can also lead to inhibition of nuclear factor-kB (NF-kB), as it affects its signaling pathway, involved in inflammation. b) Signaling pathways of inflammatory gene expressions and dietary strategies capable of modulating inflammation: Saturated fatty acids (AGS) and lipopolysaccharides (LPS) bind to toll-like receptor 4 (TLR4), which induces inflammatory responses via nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase pathways (JNK), important modulators of inflammatory gene expression. On the contrary, some food components can act by directly inhibiting these pathways. The peroxisome proliferator-activated receptor γ (PPARγ) acts by attenuating inflammation. Thus, PPARγ-binding food components may help to improve the inflammatory response.