Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
Prolonging Partial Remission in Type 1 Diabetes: The Role of Low-Carbohydrate Diet: A Literature Review.
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Rittweger de Moor Margaux, Gdoura Mariem, Lysy Philippe A
Аннотация
BACKGROUND: Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by progressive destruction of insulin-producing β-cells, resulting in lifelong insulin dependence and impaired quality of life. Although a transient phase of partial remission may occur after diagnosis, sustained preservation of β-cell function remains exceptional. Recently, low-carbohydrate diets (LCD) have gained attention among patients, partly driven by anecdotal reports describing prolonged remission.
OBJECTIVE: The aim of this review was to critically examine the existing clinical evidence for prolonged partial remission under LCD in patients with T1DM and to summarize the biological mechanisms proposed in the literature to explain such observations.
METHODS: A literature review was conducted focusing on reports of prolonged remission in individuals with T1DM adopting an LCD, as well as experimental studies exploring mechanistic pathways potentially modulated by carbohydrate restriction.
RESULTS: Only six individual cases describing prolonged partial remission under LCD were identified in the literature. The diagnostic certainty of T1DM in these reports was variable, and misclassification (eg, latent autoimmune diabetes in adults or monogenic diabetes) cannot be excluded. The mechanistic hypotheses proposed-including reduction of glucotoxicity, modulation of inflammation, attenuation of oxidative stress, and possible β-cell regeneration-are derived predominantly from animal models, in vitro studies, and non-T1DM populations. Currently, no controlled clinical trial has demonstrated that LCDs prolong remission or preserve β-cell function in patients with T1DM.
CONCLUSION: Evidence supporting prolonged partial remission under LCD in patients with T1DM remains based on rare case reports of uncertain diagnostic validity. Mechanistic data are largely indirect and extrapolated from heterogeneous experimental contexts. At present, LCD cannot be considered as a therapeutic strategy for inducing or maintaining remission in T1DM. This review highlights the need for well-designed longitudinal studies with stringent diagnostic criteria and mechanistic validation in authentic T1DM models.
OBJECTIVE: The aim of this review was to critically examine the existing clinical evidence for prolonged partial remission under LCD in patients with T1DM and to summarize the biological mechanisms proposed in the literature to explain such observations.
METHODS: A literature review was conducted focusing on reports of prolonged remission in individuals with T1DM adopting an LCD, as well as experimental studies exploring mechanistic pathways potentially modulated by carbohydrate restriction.
RESULTS: Only six individual cases describing prolonged partial remission under LCD were identified in the literature. The diagnostic certainty of T1DM in these reports was variable, and misclassification (eg, latent autoimmune diabetes in adults or monogenic diabetes) cannot be excluded. The mechanistic hypotheses proposed-including reduction of glucotoxicity, modulation of inflammation, attenuation of oxidative stress, and possible β-cell regeneration-are derived predominantly from animal models, in vitro studies, and non-T1DM populations. Currently, no controlled clinical trial has demonstrated that LCDs prolong remission or preserve β-cell function in patients with T1DM.
CONCLUSION: Evidence supporting prolonged partial remission under LCD in patients with T1DM remains based on rare case reports of uncertain diagnostic validity. Mechanistic data are largely indirect and extrapolated from heterogeneous experimental contexts. At present, LCD cannot be considered as a therapeutic strategy for inducing or maintaining remission in T1DM. This review highlights the need for well-designed longitudinal studies with stringent diagnostic criteria and mechanistic validation in authentic T1DM models.