Effect and Mechanism of Jujube on Food Intake and Intestinal Inflammatory Injury in Type 2 Diabetic Rats

Objective: To investigate the effects and underlying mechanisms of jujube on feeding behavior and intestinal inflammatory injury in rats with type 2 diabetes mellitus (T2DM). Methods: SD rats were randomly assigned to four groups: a blank control group, a T2DM model group, a low-dose jujube group (1.575 g/kg), and a high-dose jujube group (9.45 g/kg). Apart from the blank group, rats in the remaining groups were subjected to a high-fat, high-sugar diet combined with streptozotocin (STZ) administration to induce the T2DM model. Following successful model establishment, rats in the jujube groups received daily gavage with different concentrations of jujube solution for 4 consecutive weeks. General conditions, food intake, and blood glucose levels were monitored and recorded. Additionally, serum levels of inflammatory factors including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY) were assayed. Histopathological analysis of the ileum was performed to assess tissue damage and cell apoptosis, and the expressions of inflammation- and apoptosis-related genes such as nuclear factor NF-κB p65 (NF-κB p65) and cysteine-aspartic acid protease-3 (Caspase3), as well as related proteins including Toll-like receptor 4 (TLR4), NF-κB p65, phosphorylated NF-κB p65 (p-NF-κB p65), BCL2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), Pro Caspase3, and Cleaved Caspase3 were measured in the intestinal tissue. Results: Compared with the model group, the rats in the administration group exhibited a highly significant reduction in food intake (P<0.01). Serum levels of TNF-α and IL-1β were significantly decreased (P<0.01), while GLP-1 levels were markedly elevated (P<0.01). Notably, PYY levels showed a highly significant increase in the high-dose jujube group (P<0.01). Additionally, the inflammatory injury in ileal tissue improved, with a significant reduction in the apoptosis rate of ileal cells in the high-dose jujube group (P<0.01). Furthermore, the expression levels of intestinal NF-κB p65, Caspase3 mRNA, as well as NF-κB p65 and Cleaved Caspase3 proteins were significantly downregulated in the administration group (P<0.05, P<0.01). Additionally, the high-dose jujube group exhibited significant downregulation of p-NF-κB p65, Pro Caspase3, and the Bax/Bcl-2 protein ratio (P<0.05, P<0.01). Conclusion: Jujube has the potential to elevate intestinal anorexigenic hormones GLP-1 and PYY, thereby reducing food intake in T2DM rats. This effect may be mediated through jujube's ability to alleviate intestinal inflammation, repair intestinal damage, and restore intestinal hormone secretion in T2DM rats.

Publication Details

Journal
SHILAP Revista de lepidopterología
Published
2024-10-01
DOI
https://doi.org/10.13386/j.issn1002-0306.2023030333
Primary Topic
Plant pathogens and resistance mechanisms
Type
article
Field-Weighted Citation Impact
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article

Effect and Mechanism of Jujube on Food Intake and Intestinal Inflammatory Injury in Type 2 Diabetic Rats

SHILAP Revista de lepidopterología
Plant pathogens and resistance mechanisms
article

Effect and Mechanism of Jujube on Food Intake and Intestinal Inflammatory Injury in Type 2 Diabetic Rats

article en

Abstract

Objective: To investigate the effects and underlying mechanisms of jujube on feeding behavior and intestinal inflammatory injury in rats with type 2 diabetes mellitus (T2DM). Methods: SD rats were randomly assigned to four groups: a blank control group, a T2DM model group, a low-dose jujube group (1.575 g/kg), and a high-dose jujube group (9.45 g/kg). Apart from the blank group, rats in the remaining groups were subjected to a high-fat, high-sugar diet combined with streptozotocin (STZ) administration to induce the T2DM model. Following successful model establishment, rats in the jujube groups received daily gavage with different concentrations of jujube solution for 4 consecutive weeks. General conditions, food intake, and blood glucose levels were monitored and recorded. Additionally, serum levels of inflammatory factors including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY) were assayed. Histopathological analysis of the ileum was performed to assess tissue damage and cell apoptosis, and the expressions of inflammation- and apoptosis-related genes such as nuclear factor NF-κB p65 (NF-κB p65) and cysteine-aspartic acid protease-3 (Caspase3), as well as related proteins including Toll-like receptor 4 (TLR4), NF-κB p65, phosphorylated NF-κB p65 (p-NF-κB p65), BCL2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), Pro Caspase3, and Cleaved Caspase3 were measured in the intestinal tissue. Results: Compared with the model group, the rats in the administration group exhibited a highly significant reduction in food intake (P<0.01). Serum levels of TNF-α and IL-1β were significantly decreased (P<0.01), while GLP-1 levels were markedly elevated (P<0.01). Notably, PYY levels showed a highly significant increase in the high-dose jujube group (P<0.01). Additionally, the inflammatory injury in ileal tissue improved, with a significant reduction in the apoptosis rate of ileal cells in the high-dose jujube group (P<0.01). Furthermore, the expression levels of intestinal NF-κB p65, Caspase3 mRNA, as well as NF-κB p65 and Cleaved Caspase3 proteins were significantly downregulated in the administration group (P<0.05, P<0.01). Additionally, the high-dose jujube group exhibited significant downregulation of p-NF-κB p65, Pro Caspase3, and the Bax/Bcl-2 protein ratio (P<0.05, P<0.01). Conclusion: Jujube has the potential to elevate intestinal anorexigenic hormones GLP-1 and PYY, thereby reducing food intake in T2DM rats. This effect may be mediated through jujube's ability to alleviate intestinal inflammation, repair intestinal damage, and restore intestinal hormone secretion in T2DM rats.

SHILAP Revista de lepidopterología
Zero hunger
Openalex Percentile: Top 33%
Plant pathogens and resistance mechanisms
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