<![CDATA[High sugar intake, particularly from added sugars and sugar-sweetened beverages, is known to contribute to the increasing prevalence of obesity and insulin resistance, which are risk factors for various metabolic diseases. The Objective of the review to determine the relationship between high sugar intake and insulin resistance in obesity based on published research findings. This study used a literature review method by searching articles through the PubMed databases published between 2021 and 2026. Article selection was conducted based on the PRISMA 2020 guidelines, resulting in 12 articles that met the inclusion criteria. Literature synthesis demonstrates that high sugar consumption, particularly liquid fructose, drives insulin resistance through hepatic de novo lipogenesis (DNL), accumulation of toxic plasma ceramides, low-grade systemic inflammation (elevated CRP and IL-6), gut microbiota dysbiosis, and altered expression of lipogenic genes (e.g., MEG3 and FTO). Isocaloric fructose restriction studies showed significant improvements in insulin sensitivity and reduction of hepatic fat, independent of substantial weight loss. Furthermore, a bidirectional vicious cycle exists where higher baseline insulin resistance reinforces sensory preferences for sugar-sweetened foods. There is a strong and causal relationship between high sugar intake and insulin resistance in obesity, mediated by complex molecular and metabolic pathways. Restricting added sugar intake, especially from sugar-sweetened beverages, is highly recommended as a primary prevention and clinical management strategy for obesity.]]>
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