{
  "abstract": "From the triumvirate to the ominous octet and beyond, the pathophysiology of type 2 diabetes (T2D) has been progressively expanded to integrate an increasingly complex network of metabolic abnormalities.1 Nevertheless, despite these advances and the recognition of numerous additional contributors to dysglycemia, our conceptual framework for T2D in 2026 still rests on two fundamental defects: insulin resistance and progressive β-cell dysfunction. These abnormalities have shaped both our understanding of disease progression and the development of modern glucose-lowering therapies. Yet despite major advances in diabetes care, an important physiological question remains unresolved: why does glucagon secretion remain inappropriately elevated even in the presence of hyperglycemia and hyperinsulinemia?1",
  "authors": [
    {
      "affiliations": [
        "Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Mexico City, CDMX, Mexico",
        "Internal Medicine, Hospital General Dr Manuel Gea Gonzalez, Mexico City, CDMX, Mexico"
      ],
      "name": "Nubia Eréndira Ramírez-Villegas"
    },
    {
      "affiliations": [
        "Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Mexico City, CDMX, Mexico",
        "Internal Medicine, Hospital General Dr Manuel Gea Gonzalez, Mexico City, CDMX, Mexico"
      ],
      "name": "Froylan David Martínez-Sánchez"
    }
  ],
  "title": "From beta-cell failure to islet dysfunction: the emerging role of the alpha cell",
  "uid": "30f87c1a-2afc-58be-8d7c-df447faf7f34"
}