# Nutritional Interventions in Type 1 Diabetes: Boosting Residual GLP-1 Responses—Is It an Option?

**Authors:** Maria Grammatiki, Xanthippi Tsekmekidou, Theocharis Koufakis, Kalliopi Kotsa

PMC · DOI: 10.3390/nu18040564 · Nutrients · 2026-02-09

## TL;DR

This paper explores how dietary and lifestyle changes might boost GLP-1 responses in early-stage Type 1 Diabetes to preserve beta-cell function and improve glycemic control.

## Contribution

The paper introduces the novel idea of using nutritional interventions to enhance residual GLP-1 signaling in early-stage Type 1 Diabetes.

## Key findings

- High-fiber diets may increase GLP-1 via microbiota-derived short-chain fatty acids.
- Mediterranean diets may promote GLP-1 secretion through fiber, polyphenols, and unsaturated fatty acids.
- Low-glycemic index carbohydrates may favor GLP-1-dominant incretin profiles.

## Abstract

Type 1 diabetes (T1D) is characterized by autoimmune beta-cell destruction and lifelong insulin dependence, yet early-stage disease (Stages 1–2) retains residual beta-cell function that may still respond to incretin signaling. Incretin hormones—mainly glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)—enhance postprandial insulin secretion and suppress glucagon, and GLP-1 also exhibits beta-cell protective effects in preclinical models. Although the incretin effect is markedly reduced in established T1D, intestinal GLP-1 secretion is largely preserved, creating a mechanistic rationale for strategies that increase endogenous GLP-1 during the “residual function” window. This narrative review summarizes dietary and lifestyle interventions that may enhance endogenous GLP-1 responses and discusses their potential role as adjuncts to insulin therapy, particularly when combined with emerging beta-cell-preserving immunomodulatory approaches that may prolong early disease stages. Mechanistically, high-fiber diets may increase GLP-1 via microbiota-derived short-chain fatty acids acting on L-cell receptors; low-glycemic index carbohydrates may favor distal nutrient delivery and a GLP-1-dominant incretin profile; and Mediterranean dietary patterns may promote GLP-1 secretion through unsaturated fatty acids, fiber, and polyphenols, including potential DPP-4-modulating effects. This narrative review examines nutrition and lifestyle interventions modulating residual incretins to elongate early T1D stages and enhance glycemic control as insulin adjuncts, per Nutrients’ Special Issue. Available evidence is strongest in non-T1D populations, with limited T1D-specific trials, highlighting the need for stage-targeted studies incorporating GLP-1 dynamics, C-peptide, glycemic variability, and microbiome outcomes.

## Linked entities

- **Proteins:** GCG (glucagon), GIP (gastric inhibitory polypeptide)
- **Diseases:** Type 1 diabetes (MONDO:0005147), T1D (MONDO:0005147)

## Full-text entities

- **Genes:** FFAR4 (free fatty acid receptor 4) [NCBI Gene 338557] {aka BMIQ10, GPR120, GPR129, GT01, O3FAR1, OB10Q}, GIP (gastric inhibitory polypeptide) [NCBI Gene 2695], FFAR3 (free fatty acid receptor 3) [NCBI Gene 2865] {aka FFA3R, GPR41}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, Gcg (glucagon) [NCBI Gene 24952] {aka GLP-1, Glp1, Glp2}, GCG (glucagon) [NCBI Gene 2641] {aka GLP-1, GLP1, GLP2, GRPP}, DPP4 (dipeptidyl peptidase 4) [NCBI Gene 1803] {aka ADABP, ADCP2, CD26, DPPIV, TP103}, FFAR2 (free fatty acid receptor 2) [NCBI Gene 2867] {aka FFA2R, GPR43}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** T1D (MESH:D003922), overweight (MESH:D050177), obese (MESH:D009765), autoimmune disease (MESH:D001327), T2D (MESH:D003924), fatty liver (MESH:D005234), impaired glucose tolerance (MESH:D018149), metabolic disorders (MESH:D008659), hyperglycemia (MESH:D006943), inflammatory (MESH:D007249), gastrointestinal symptoms (MESH:D012817), injury to (MESH:D014947), insulin deficiency (MESH:D007333), pancreatic insulitis (MESH:D010195), prediabetes (MESH:D011236), diabetes (MESH:D003920), cardiovascular disease (MESH:D002318), hypoglycemia (MESH:D007003)
- **Chemicals:** STZ (MESH:D013311), sucrose (MESH:D013395), lipid (MESH:D008055), Polyphenols (MESH:D059808), amide (MESH:D000577), FA (MESH:D005492), calcium (MESH:D002118), SCFA (MESH:D005232), blood glucose (MESH:D001786), beta-glucan (MESH:D047071), cholesterol (MESH:D002784), C-peptide (MESH:D002096), Isomaltulose (MESH:C008189), glucose (MESH:D005947), Inulin (MESH:D007444), Teplizumab (MESH:C502540), Acetate (MESH:D000085), maltodextrin (MESH:C008315), oligofructose (MESH:C120489), polyunsaturated fatty acids (MESH:D005231), sugars (MESH:D000073893), -Fiber (MESH:D004043), olive oil (MESH:D000069463), ITF (-), fatty acids (MESH:D005227), Carbohydrates (MESH:D002241), monounsaturated fatty acids (MESH:D005229), phytosterols (MESH:D010840), propionate (MESH:D011422), triglyceride (MESH:D014280), butyrate (MESH:D002087)
- **Species:** Brassica oleracea var. italica (asparagus broccoli, varietas) [taxon 36774], Solanum tuberosum (potatoes, species) [taxon 4113], Lens culinaris (lentil, species) [taxon 3864], Lathyrus oleraceus (garden pea, species) [taxon 3888], Malus domestica (apple, species) [taxon 3750], Akkermansia muciniphila (species) [taxon 239935], Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Cell lines:** L- — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0462)

## Full text

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## Figures

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## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC12943052/full.md

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Source: https://tomesphere.com/paper/PMC12943052