Liliana Muñoz-Hernández1,2, Ziomara Márquez-López1, Roopa Mehta1, Carlos Alberto Aguilar-Salinas3,4,5. 1. Metabolic Diseases Research Unit, Instituto Nacional de Ciencias Medicas y Nutricion, Mexico City, Mexico. 2. Consejo Nacional de Ciencia y Tecnología, Mexico City, Mexico. 3. Metabolic Diseases Research Unit, Instituto Nacional de Ciencias Medicas y Nutricion, Mexico City, Mexico. caguilarsalinas@yahoo.com. 4. Escuela de Medicina y Ciencias de la Salud, Tecnológico de Monterrey, Monterrey, Mexico. caguilarsalinas@yahoo.com. 5. Division of Nutrition, Instituto Nacional de Ciencias Medicas y Nutricion, Vasco de Quiroga #15, Tlalpan, 14080, Mexico City, Mexico. caguilarsalinas@yahoo.com.
Abstract
PURPOSE OF REVIEW: Diet is a pillar of type 2 diabetes mellitus (T2DM) management. Intermittent fasting (IF) is postulated as a novel approach, able to improve glucose control and potentially capable of reversing some of the pathophysiological alterations of this condition. In this review, the molecular and clinical evidence of diets based on intermittent energy restriction (IER) in laboratory animal models and subjects with type 2 diabetes is discussed. The mechanisms through which IF are thought to improve glucose homeostasis and reverse β cell failure are also reviewed. RECENT FINDINGS: Studies derived from murine models suggest that IER is associated with improvements in β cell function and insulin resistance. Two main mechanisms have been demonstrated, one derived from the autophagy-lysosome pathway and, the other from an increase in neurogenin3 (Ngn3) levels (a marker for endocrine progenitor cells like β cells during development). Notably, IER also promotes reconstruction of gut microbiota. In mice, all effects were independent of weight loss. By contrast, in human studies, outcomes are widely attributable to weight loss. The more consistent results are reductions in body weight, visceral fat, and glucose and insulin levels. Increases in HDL cholesterol levels are also frequently reported. The decrease in insulin levels observed in humans is in opposition with the increase reported in mice, suggesting that the main mechanism in humans is an improvement in peripheral insulin action. Recommending diets based on intermittent fasting in humans is based on the promising results found in animal models where an improvement in β cell function has been recorded. β cell function after IF has not been assessed in human subjects with T2DM. This review provides information regarding different protocols for the implementation of IF in diabetic persons and also provides important safety advice in order to avoid adverse effects. Clinical studies do not show an increased risk of hypoglycemia, and a recent case series reported reversal of T2DM.
PURPOSE OF REVIEW: Diet is a pillar of type 2 diabetes mellitus (T2DM) management. Intermittent fasting (IF) is postulated as a novel approach, able to improve glucose control and potentially capable of reversing some of the pathophysiological alterations of this condition. In this review, the molecular and clinical evidence of diets based on intermittent energy restriction (IER) in laboratory animal models and subjects with type 2 diabetes is discussed. The mechanisms through which IF are thought to improve glucose homeostasis and reverse β cell failure are also reviewed. RECENT FINDINGS: Studies derived from murine models suggest that IER is associated with improvements in β cell function and insulin resistance. Two main mechanisms have been demonstrated, one derived from the autophagy-lysosome pathway and, the other from an increase in neurogenin3 (Ngn3) levels (a marker for endocrine progenitor cells like β cells during development). Notably, IER also promotes reconstruction of gut microbiota. In mice, all effects were independent of weight loss. By contrast, in human studies, outcomes are widely attributable to weight loss. The more consistent results are reductions in body weight, visceral fat, and glucose and insulin levels. Increases in HDL cholesterol levels are also frequently reported. The decrease in insulin levels observed in humans is in opposition with the increase reported in mice, suggesting that the main mechanism in humans is an improvement in peripheral insulin action. Recommending diets based on intermittent fasting in humans is based on the promising results found in animal models where an improvement in β cell function has been recorded. β cell function after IF has not been assessed in human subjects with T2DM. This review provides information regarding different protocols for the implementation of IF in diabeticpersons and also provides important safety advice in order to avoid adverse effects. Clinical studies do not show an increased risk of hypoglycemia, and a recent case series reported reversal of T2DM.
Entities:
Keywords:
Alternate-day fasting; Fasting-mimicking diets; Intermittent energy restriction; Intermittent fasting; Time-restricted feeding; Type 2 diabetes remission
Authors: Solomon A Sowah; Alessio Milanese; Ruth Schübel; Jakob Wirbel; Ece Kartal; Theron S Johnson; Frank Hirche; Mirja Grafetstätter; Tobias Nonnenmacher; Romy Kirsten; Marina López-Nogueroles; Agustín Lahoz; Kathrin V Schwarz; Jürgen G Okun; Cornelia M Ulrich; Johanna Nattenmüller; Arnold von Eckardstein; Daniel Müller; Gabriele I Stangl; Rudolf Kaaks; Tilman Kühn; Georg Zeller Journal: Genome Med Date: 2022-03-14 Impact factor: 11.117