# Appetite and its Regulation: Are there Palatable Interventions for Heart Failure?

**Authors:** Matthew M. Y. Lee, Michael E. J. Lean, Naveed Sattar, Mark C. Petrie

PMC · DOI: 10.1007/s11897-023-00637-7 · Current Heart Failure Reports · 2023-12-22

## TL;DR

This paper explores how managing appetite and weight through diet, medications, or surgery can help treat heart failure, with promising results from new drugs like glucagon-like peptide-1 receptor agonists.

## Contribution

The paper highlights the potential of appetite-regulating medications, particularly glucagon-like peptide-1 receptor agonists, in managing heart failure through weight loss.

## Key findings

- Glucagon-like peptide-1 receptor agonists can significantly reduce appetite and achieve substantial weight loss.
- The STEP-HFpEF trial showed meaningful improvements in health status for heart failure patients.
- Weight loss interventions may complement existing heart failure treatments.

## Abstract

Obesity is a major driver of heart failure (HF) incidence, and aggravates its pathophysiology. We summarized key reported and ongoing randomized clinical trials of appetite regulation and/or dietary energy restriction in individuals with HF.

Weight loss can be achieved by structured supervised diet programs with behavioural change, medications, or surgery. The new glucagon-like peptide-1 receptor agonists alone or in combination with other agents (e.g., glucose-dependent insulinotropic polypeptide and glucagon receptor agonists or amylin analogues) potently and sustainably reduce appetite, and, taken together with dietary advice, can produce substantial, life-changing, weight loss approaching that achieved by surgery. To date, data from the STEP-HFpEF trial show meaningful improvements in health status (Kansas City Cardiomyopathy Questionnaire).

Effective weight management could relieve several drivers of HF, to complement the existing treatments for HF with both reduced and preserved ejection fraction. Further trials of weight loss interventions will provide more definitive evidence to understand their effects on clinical events in patients with HF.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252), HF (MONDO:0015193)

## Full-text entities

- **Genes:** GCGR (glucagon receptor) [NCBI Gene 2642] {aka GGR, GL-R, MVAH}, GCG (glucagon) [NCBI Gene 2641] {aka GLP-1, GLP1, GLP2, GRPP}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, GIP (gastric inhibitory polypeptide) [NCBI Gene 2695], CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** Cardiomyopathy (MESH:D009202), HF with preserved ejection fraction (MESH:D054144), Weight Loss (MESH:D015431), Diabetes (MESH:D003920), inflammation (MESH:D007249), dumping syndrome (MESH:D004377), HF (MESH:D006333), cardiovascular deaths (MESH:D002318), restriction (MESH:D002313), Obesity (MESH:D009765), HF with reduced ejection fraction (MESH:D054143), vitamin and mineral deficiencies (MESH:C537337)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC10827951/full.md

## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC10827951/full.md

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Source: https://tomesphere.com/paper/PMC10827951