# Weight Loss by Diet Versus Metabolic Surgery Increases Circulating NT-proANP in Obese Individuals

**Authors:** Andreas Schmid, Maria Koukou, Thomas Karrasch, Andreas Schäffler

PMC · DOI: 10.3390/jcm15041515 · Journal of Clinical Medicine · 2026-02-14

## TL;DR

Weight loss through diet or surgery increases NT-proANP levels in obese individuals, suggesting a role in metabolic regulation.

## Contribution

The study shows that weight loss increases NT-proANP levels regardless of the therapy used, providing new insight into metabolic regulation.

## Key findings

- NT-proANP levels significantly increased during weight loss over 12 months in both diet and surgery groups.
- NPRA expression was higher in visceral compared to subcutaneous adipose tissue.
- NT-proANP levels correlated with fibroblast growth factors 19 and 21 at baseline.

## Abstract

Background: Natriuretic peptides are endocrine factors that regulate various physiological processes via natriuretic peptide receptors (NPRs). Regulation of the atrial natriuretic peptide ANP during weight loss remains widely unknown. The present study investigated serum quantities of the circulating ANP precursor NT-proANP in obesity and during therapy-induced weight loss. Methods: The study enrolled 284 severely obese individuals. A total of 163 patients underwent metabolic surgery (either Roux-en-Y gastric bypass or vertical sleeve gastrectomy) and 121 patients participated in a non-invasive obesity therapy applying low-calorie formula diet. Anthropometric and physiological data were assessed, and blood serum was prepared at study baseline and at follow-up visits (3 and 12 months after start of intervention). Subcutaneous and visceral adipose tissue specimen were obtained from metabolic surgery patients. Circulating NT-proANP levels were determined by ELISA and gene expression levels of the receptor NPRA in adipose tissue were quantified by real-time RT-PCR. Results: Comparative analysis revealed significantly higher NPRA expression in visceral than in subcutaneous adipose tissue. NT-proANP levels significantly increased during weight loss over 12 months upon diet and metabolic surgery. NT-proANP serum concentrations were positively correlated with fibroblast growth factors 19 and 21 quantities at study baseline and considerably increased during weight loss in both cohorts after 12 months. We conclude that weight loss is a positive regulator of circulating NT-proANP quantities, regardless of the applied therapy.

## Linked entities

- **Genes:** NPR1 (natriuretic peptide receptor 1) [NCBI Gene 4881]
- **Proteins:** NPPA (natriuretic peptide A)
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** GRN (granulin precursor) [NCBI Gene 2896] {aka CLN11, FTD2, GEP, GP88, PCDGF, PEPI}, C1QTNF3 (C1q and TNF related 3) [NCBI Gene 114899] {aka C1ATNF3, CORCS, CORS, CORS-26, CORS26, CTRP3}, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, NPR2 (natriuretic peptide receptor 2) [NCBI Gene 4882] {aka AMDM, ANPRB, ANPb, ECDM, GC-B, GCB}, PPRC1 (PPARG related coactivator 1) [NCBI Gene 23082] {aka PRC}, NPPA (natriuretic peptide A) [NCBI Gene 4878] {aka ANF, ANP, ATFB6, ATRST2, CDD, CDD-ANF}, METRNL (meteorin like, glial cell differentiation regulator) [NCBI Gene 284207], Gapdh (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 14433] {aka Gapd}, FGF19 (fibroblast growth factor 19) [NCBI Gene 9965], CAMP (cathelicidin antimicrobial peptide) [NCBI Gene 820] {aka CAP-18, CAP18, CRAMP, FALL-39, FALL39, HSD26}, ADRB3 (adrenoceptor beta 3) [NCBI Gene 155] {aka BETA3AR}, NPR1 (natriuretic peptide receptor 1) [NCBI Gene 4881] {aka ANP-A, ANPRA, ANPa, GC-A, GUC2A, GUCY2A}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, CNP (2',3'-cyclic nucleotide 3' phosphodiesterase) [NCBI Gene 1267] {aka CN37, CNP1, HLD20}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, FGF21 (fibroblast growth factor 21) [NCBI Gene 26291], INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** Obese (MESH:D009765), type 2 diabetes (MESH:D003924), LCD (MESH:D011502), caloric restriction (MESH:D002313), metabolic dysregulation (MESH:D021081), bulimia nervosa (MESH:D052018), ventricular fibrosis (MESH:D005355), metabolic syndrome (MESH:D024821), injury to (MESH:D014947), adipose inflammation (MESH:D007249), hypertension (MESH:D006973), dyslipidemia (MESH:D050171), BS (MESH:D000267), diabetes mellitus (MESH:D003920), neoplasm (MESH:D009369), endocrine diseases (MESH:D004700), psychosis (MESH:D011618), psychiatric disorders (MESH:D001523), insulin resistance (MESH:D007333), Weight Loss (MESH:D015431), binge eating behavior (MESH:D002032)
- **Chemicals:** eicosapentaenoic acid (MESH:D015118), H2O. (MESH:D014867), TRIzol (MESH:C411644), margarinic acid (MESH:C013102), docosahexaenoic acid (MESH:D004281), chloroform (MESH:D002725), lipid (MESH:D008055), oligonucleotides (MESH:D009841), oleic acid (MESH:D019301), myristic acid (MESH:D019814), linoleic acid (MESH:D019787), bile acids (MESH:D001647), fat (MESH:D005223), NT-proANP (-), salt (MESH:D012492), lactose (MESH:D007785), catecholamine (MESH:D002395), Natriuretic peptides (MESH:D045265), carbohydrates (MESH:D002241), fatty acids (MESH:D005227)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** A1C

## Full text

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## Figures

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## References

26 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942638/full.md

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Source: https://tomesphere.com/paper/PMC12942638