Your topics. New publications.

A compact browser notification when there’s something new. At most once a day — no account needed.

What interests you?

Optional and switchable off here at any time. We save your selected topics and device subscription; no email address is required. Privacy

Search the harborEN/DEAccount
Nutrition foundations
Research brief

Review of sweet-taste T1R2/T1R3 signalling and energy and body-weight control

This review examines how the sweet-taste receptors T1R2 and T1R3 relate to energy (glucose) and body-weight homeostasis, including their extra-oral expression in metabolically active tissues and possible use as therapeutic targets. [1]

Automatic summary · not editorially reviewed

The key findings

  1. Sweet taste perception depends on the recognition threshold for mono- and disaccharides, and threshold differences are mainly attributed to T1R2/T1R3 polymorphisms and their expression in taste buds, regulated by several hormones. [1]

  2. Aging, diabetes and obesity are characterized by significant changes in the sweet taste threshold, which can influence food intake; anti-obesity interventions are also associated with changes in sweet taste perception. [1]

  3. Extra-oral T1R expression has been identified in metabolically active tissues, with demonstrated involvement in glycaemic and body-weight control; the review discusses T1Rs as possible prevention and therapeutic targets. [1]

The source at a glance

Study type / format
Review (abstract only)
Population / context
People and metabolically active tissues discussed in a review of sweet-taste T1R2/T1R3 signalling
Summary based on
Study abstract
Original publication
September 28, 2026

Sweet threshold variation and its hormonal regulation

The abstract states that sweet taste perception depends on the recognition threshold for mono- and disaccharides. Differences in this sweet threshold are mainly attributed to polymorphisms of T1R2 and T1R3 and to their expression in taste buds, which several hormones regulate, including glucagon, ghrelins, glucagon-like peptide, leptins and endocannabinoids. The review frames these points as background to its analysis of T1R signalling.

Supporting source [1]

Sweet threshold changes in aging, diabetes and obesity

According to the abstract, aging, diabetes and obesity are characterized by significant changes in the sweet taste threshold. These changes can influence food intake and thereby contribute to the development of these pathologies. The abstract also reports that anti-obesity interventions such as caloric restriction, bariatric surgery and pharmacological treatments are associated with changes in sweet taste perception. These are described associations, not established causes.

Supporting source [1]

Extra-oral T1R expression and proposed therapeutic targets

The abstract states that extra-oral expression of T1Rs has been identified in different metabolically active tissues and that their involvement in glycaemic control and body-weight control has been demonstrated. The review analyses the physiological and pathophysiological role of T1Rs in energy homeostasis and body weight and the possibility of using them in prevention of the mentioned high-prevalence diseases and as new therapeutic targets. These are proposed possibilities, not validated treatments.

Supporting source [1]

How to interpret this

This explainer is based only on the abstract; the full text was not reviewed. The abstract reports no study design, sample, follow-up or effect sizes, and the described relationships are associations, not proven causes. Proposed therapeutic uses are not validated treatments.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    sweet taste perception is dependent of the
  2. Finding 2 ↑

    aging, diabetes and obesity are characterized by
  3. Finding 3 ↑

    extra-oral expression of T1Rs have been identified

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

Discussion

Community discussions

0 topics

Member contributions. Share sources, disclose commercial interests, and avoid personal medical or dosing advice.

Loading…