Heterogeneity-Based Decoupling of the Obesity–Type 2 Diabetes Comorbidity Association: A Dual-Channel Model Based on "Absorption–Storage Rate Mismatch"

Obesity is a recognized risk factor for type 2 diabetes mellitus (T2DM), but the BMI–T2DM association is often attenuated in large epidemiological studies, creating an illusion of an “unclear association.” This paradox may partly arise because the crude indicator “obesity” masks essential differences among pathogenic pathways. Focusing on “carbohydrate-driven obesity,” this article proposes an “absorption–storage rate mismatch” hypothesis: after refined carbohydrate intake, rapid absorption (1–2 h) exceeds limited glycogen storage rate and dynamic buffering capacity, leading to postprandial energy overflow; insulin switches on hepatic de novo lipogenesis (DNL), and visceral adipose tissue, acting as a high-throughput “emergency buffer,” accumulates rapidly and preferentially; when visceral fat reaches capacity, it releases nutrient overload-related signals (traditionally called inflammatory factors), causing graded hepatic insulin downregulation, persistent gluconeogenesis, round-the-clock pancreatic compensation, and ultimately β-cell failure and T2DM. Dietary fat storage serves as a comparator: it depends mainly on lipoprotein lipase (LPL) and does not directly require insulin; however, hyperinsulinemia upregulates LPL activity and promotes fatty acid esterification, accelerating storage. Thus, a mixed diet may double-hit: carbohydrates produce fat via DNL and indirectly promote dietary fat storage via hyperinsulinemia. Additionally, refined carbohydrates may increase caloric intake via rapid postprandial glucose declines that affect later hunger, especially in those preferring sweets/refined starch. Combining populations with different metabolic drivers may cause an epidemiological “dilution effect.” The DiRECT dose–response between weight loss and remission, and C-peptide as a staging marker, indirectly support this framework. This article predicts that, with identical calories and macronutrients, reducing input rate (e.g., smaller, more frequent meals) may benefit those with a rate bottleneck more, with a glycemic variability improvement gradient of “healthy < prediabetes < diabetes”; this requires prospective validation adjusting for baseline MAGE. This article is a theoretical hypothesis intended to propose testable propositions, not a systematic review.