Morphological alteration of the pancreatic islet in ovariectomized rats fed a high-fat high-fructose diet
Issued Date
2022-04-01
Resource Type
ISSN
09486143
eISSN
1432119X
Scopus ID
2-s2.0-85123076181
Pubmed ID
35037128
Journal Title
Histochemistry and Cell Biology
Volume
157
Issue
4
Start Page
427
End Page
442
Rights Holder(s)
SCOPUS
Bibliographic Citation
Histochemistry and Cell Biology Vol.157 No.4 (2022) , 427-442
Suggested Citation
Chansela P., Potip B., Weerachayaphorn J., Kangwanrangsan N., Chukijrungroat N., Saengsirisuwan V. Morphological alteration of the pancreatic islet in ovariectomized rats fed a high-fat high-fructose diet. Histochemistry and Cell Biology Vol.157 No.4 (2022) , 427-442. 442. doi:10.1007/s00418-021-02062-0 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/83791
Title
Morphological alteration of the pancreatic islet in ovariectomized rats fed a high-fat high-fructose diet
Author's Affiliation
Other Contributor(s)
Abstract
Diabetes and its complications are major causes of mortality worldwide. Type 2 diabetes coexists with insulin resistance and β-cell dysfunction, which are aggravated by overconsumption and estrogen-deprived conditions. However, the morphology of pancreatic islets in a combined condition of excessive caloric intake and estrogen deficiency has never been described. Herein, we examined morphological changes in the pancreatic islets of ovariectomized (OVX) rats fed a high-fat high-fructose diet (HFFD) for 12 weeks. The histological changes in the size and number of pancreatic islets were assessed by hematoxylin–eosin and immunohistochemical staining. Enlarged pancreatic islets with fat deposition in OVX rats were accompanied by whole-body insulin resistance and hyperglycemia. The addition of a HFFD to OVX rats (OVX + HFFD) further aggravated insulin resistance, with a substantial increase in the density of enlarged pancreatic islets and fat accumulation. The augmented number of enlarged islets was correlated with elevated plasma glucose and insulin levels. Intriguingly, unlike the HFFD and OVX alone, the OVX + HFFD markedly expanded the area of insulin-producing β-cells and glucagon-producing α-cells. Importantly, enlarged islets, pancreatic fat deposits, and diabetic states developing in OVX + HFFD conditions were resolved by estrogen replacement. Collectively, the morphological characteristics of pancreatic islets were influenced in an insulin-resistant state caused by estrogen deficiency and HFFD consumption and were distinct from each factor alone. A combination of estrogen deficiency with HFFD consumption worsened the integrity of pancreatic islets, ultimately resulting in disease progression. These findings expand our understanding of the causal relationship between pancreatic morphology and diabetes development and suggest therapeutic strategies.