In recent years, obesity has emerged as a significant risk factor jeopardizing human health and stands out as an urgent issue demanding attention from the global public health sector. The factors influencing obesity are intricate, making it challenging to comprehensively elucidate its causes. Recent studies indicate that food reward significantly contributes to the genesis and progression of obesity. Food reward comprises three integral components: hedonic value (liking), eating motivation (wanting), and learning and memory. Each facet is governed by the corresponding neural pathway. The mesocorticolimbic system (MS) plays a pivotal role in regulating food reward, wherein the MS encompasses dopamine (DA) neurons originating from the ventral tegmental area (VTA) projecting into various brain regions or nuclei such as the nucleus accumbens (NAc), prefrontal cortex (PFC), amygdala, and hippocampus. On one hand, prolonged consumption of palatable foods induces adaptive alterations and synaptic remodeling in neural circuits regulating food reward. This includes the attenuation of neuronal connections and signal transmission among the PFC, visual cortex, hypothalamus, midbrain, and brain stem, resulting in aberrant food reward and compelling the body to compensate for satisfaction deficiency by increasing food consumption. Studies involving humans and animals reveal that compulsive eating bears resemblance to the behavior observed in individuals with substance addictions, encompassing aspects such as food cravings, loss of eating control, and dieting failures. Propelled by food reward, individuals often opt for their preferred palatable foods during meals, potentially leading to excessive energy intake. Coupled with a sedentary lifestyle, this surplus energy is stored in the body, transforming into fat and culminating in obesity. While evidence supports the notion that prolonged exposure to a high-energy-density diet contributes to abnormal food reward, the internal mechanisms remain somewhat unclear. In previous research on depression, substance abuse, and alcohol dependence, it has been confirmed that there is a close connection between inflammation and reward. For example, obese people show a higher tendency toward depression, and white blood cell count is an important mediating variable between intake and depressive symptoms. In addition, it has been found in individuals with alcohol dependence and drug abuse that long-term opioid overdose or alcohol abuse will activate glial cells to release pro-inflammatory cytokines that affect neuronal function, and disrupt synaptic transmission of neurotransmitters to promote addictive behaviors. Comprehensive analysis suggests that inflammation may play an important role in the reward regulation process. Recent studies indicate that metaflammation within the central or peripheral system, triggered by excess nutrients and energy, can disrupt the normal transmission of reward signals. This disruption affects various elements, such as DA signaling (synthesis, release, reuptake, receptor function, and expression), mu opioid receptor function, glutamate excitatory synaptic transmission, Toll-like receptor 4 (TLR4) signal activation, and central insulin/leptin receptor signal transduction. Consequently, this disruption induces food reward dysfunction, thereby fostering the onset and progression of obesity. Building upon these findings, we hypothesized that obesity may be linked to abnormal food reward induced by metaflammation. This review aims to delve deeply into the intricate relationship between obesity, food reward, and metaflammation. Additionally, it seeks to summarize the potential mechanisms through which metaflammation induces food reward dysfunction, offering novel insights and a theoretical foundation for preventing and treating obesity.