# Pancreatic functions in high salt fed female rats

**Authors:** Noha N Lasheen

PMC · DOI: 10.14814/phy2.12443 · Physiological Reports · 2015-07-26

## TL;DR

This study shows that a high salt diet in female rats leads to pancreatic fibrosis and reduced pancreatic function.

## Contribution

The study reveals the negative impact of high salt diets on both exocrine and endocrine pancreatic functions in rats.

## Key findings

- High salt diet caused significant increases in body weight, BMI, Lee index, plasma sodium, TGF-β1, and IL6.
- Pancreatic fibrosis was observed in the high salt-fed group with reduced amylase, lipase, aldosterone, and insulin levels.
- No significant changes in fasting blood glucose or HOMA-IR were found between the groups.

## Abstract

Salt consumption has been increased worldwide and the association of high salt diets with enhanced inflammation and target organ damage was reported. Little data were available about the effect of high salt diet on exocrine function of pancreas, while the relation between high salt intake and insulin sensitivity was controversial. This study was designed to investigate the effect of high salt diet on exocrine and endocrine pancreatic functions, and to elucidate the possible underlying mechanism(s). Twenty adult female Wistar rats were randomly divided into two groups; control group; fed standard rodent diet containing 0.3% NaCl, and high salt fed group; fed 8% NaCl for 8 weeks. On the day of sacrifice, rats were anesthized by i.p. pentobarbitone (40 μg/kg B.W.). Nasoanal length was measured and fasting blood glucose was determined from rat tail. Blood samples were obtained from abdominal aorta for determination of plasma sodium, potassium, amylase, lipase, aldosterone, insulin, transforming growth factor-β (TGF-β1), and interleukin 6 (IL6). Pancreata of both groups were histologically studied. Compared to control group, 8-week high salt fed group showed: significant elevation in body weight, body mass index, Lee index, plasma sodium, TGF-β1 and IL6, however, plasma aldosterone, amylase, lipase, and insulin levels were significantly decreased. A nonsignificant increase in plasma potassium and nonsignificant changes in fasting blood glucose and HOMA-IR were detected between groups. Pancreatic fibrosis was observed in test group. High salt diet for 8 weeks caused pancreatic fibrosis evidenced by decline of both exocrine and endocrine functions of pancreas in Wistar rats.

## Linked entities

- **Proteins:** TGFB1 (transforming growth factor beta 1), IL6 (interleukin 6), PIN (insulin precursor), amylase (pancreatic alpha-amylase-like), lipase (lipase)
- **Chemicals:** NaCl (PubChem CID 5234), pentobarbitone (PubChem CID 4737)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, Ren (renin) [NCBI Gene 24715] {aka RATRENAA, RENAA, Ren1}, NR3C2 (nuclear receptor subfamily 3 group C member 2) [NCBI Gene 4306] {aka MCR, MLR, MR, NR3C2VIT}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 59086] {aka Tgfb}, Fn1 (fibronectin 1) [NCBI Gene 25661] {aka FIBNEC, fn-1}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, Lipg (lipase G, endothelial type) [NCBI Gene 291437] {aka lipase}, Nr3c1 (nuclear receptor subfamily 3, group C, member 1) [NCBI Gene 24413] {aka GR, Gcr, Grl}, Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}, Stat1 (signal transducer and activator of transcription 1) [NCBI Gene 25124] {aka DD6G4-4}, Gcg (glucagon) [NCBI Gene 24952] {aka GLP-1, Glp1, Glp2}, AGT (angiotensinogen) [NCBI Gene 183] {aka ANHU, SERPINA8, hFLT1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** hypertrophy (MESH:D006984), chronic pancreatitis (MESH:D050500), organ failure (MESH:D009102), impairment of exocrine pancreatic function (MESH:C565225), C.T (MESH:D001260), endocrine dysfunction (MESH:D004700), Pancreatic ductal stenosis (MESH:D021441), obesity (MESH:D009765), exocrine and endocrine pancreatic insufficiency (MESH:D010188), inflammation (MESH:D007249), endocrine failure (MESH:D051437), lipid disorders (MESH:D011017), tissue injury (MESH:D017695), insulin deficiency (MESH:D007333), type 2 diabetes mellitus (MESH:D003924), decline in renal function (MESH:D060825), abnormal glucose tolerance (MESH:D018149), and renal (MESH:D006030), hypertension (MESH:D006973), cardiovascular disease (MESH:D002318), pancreatic damage (MESH:D010182), diabetes mellitus (MESH:D003920), cardiac, vascular, and renal hypertrophy (MESH:D006332), function (MESH:D003291), Fibrosis of pancreas (MESH:D003550), target organ damage (MESH:D000092124), hearts (MESH:D006331), kidneys (MESH:D007674), Fibrosis (MESH:D005355), Pancreatic endocrine deficiency (MESH:D010195), insulin-dependent diabetes mellitus (MESH:D003922), destruction (MESH:D008105), vascular injury (MESH:D057772), left ventricular hypertrophy (MESH:D017379)
- **Chemicals:** nitric oxide (MESH:D009569), Na+ (MESH:D012964), uric acid (MESH:D014527), reactive oxygen species (MESH:D017382), ethanol (MESH:D000431), Aldosterone (MESH:D000450), blood glucose (MESH:D001786), Salt (MESH:D012492), glucose (MESH:D005947), K+ (MESH:D011188), Nasoanal (-), formalin (MESH:D005557), fructose (MESH:D005632), NaCl (MESH:D012965), H&amp;E (MESH:D006371), water (MESH:D014867), Pentobarbital (MESH:D010424), spironolactone (MESH:D013148)
- **Species:** Bos taurus (bovine, species) [taxon 9913], Mus musculus (house mouse, species) [taxon 10090], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** H&amp;E — Homo sapiens (Human), Transformed cell line (CVCL_ZD53)

## Full text

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## Figures

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## References

53 references — full list in the complete paper: https://tomesphere.com/paper/PMC4552525/full.md

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Source: https://tomesphere.com/paper/PMC4552525