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RVC PhD: Investigating the role of gut microbiota in feline diabetes mellitus and hypersomatotropism


Project Description

Diabetes mellitus (DM) is a common feline endocrinopathy, estimated to affect 1 in 200 cats examined in UK primary-care practice. Feline DM often resembles type 2 DM in people but, in approximately 25% of cases, DM in cats can also develop secondary to underlying hypersomatotropism (HS). In cats with HS, DM primarily results from severe insulin resistance from excessive growth hormone production from a pituitary tumour. In contrast, cats with type 2-like DM likely have a more heterogenous DM pathogenesis including β-cell dysfunction, genetic influences and diabetogenic factors, such as obesity. Populations of cats with type 2-like DM are therefore highly diverse, which could account for why therapeutic interventions studied to date have yielded very divergent outcomes and predictors of treatment response. Feline type-2 like DM is also characterized by the potential for ‘diabetic remission’ due to recovery of β-cell function and / or reduction in insulin resistance following a period of insulin therapy.

The role of the intestinal microbiota in the pathogenesis of human type 2 DM and its potential as a therapeutic target is being increasingly recognised. However, only two studies have compared the gut microbiome of diabetic and non-diabetic cats, yielding contrasting results. This could have resulted from a number of study limitations, including lack of dietary standardization and limitations in the 16S rRNA technique used. It is also not clear whether the microbiome of cats with type 2-like DM is similar to that of cats with DM secondary to HS, nor whether changes in the microbiome are associated with the attainment of diabetic remission in cats. Dissecting these important differences will be crucial in the exploration of the microbiome as a potential therapeutic target in diabetic cats.

This project will use advanced high throughput sequencing and metabolomics techniques to evaluate the microbiome and metabolome among diabetic cats,
1) with and without HS
2) at times of poor and good glycaemic control
3) before and after they achieve diabetic remission
4) in comparison to non-diabetic healthy cats.

As well as recruiting cases via the RVC’s Diabetic Remission Clinic, the successful candidate will receive training in laboratory techniques, bioinformatics and data analysis and will join a thriving diabetes research community at the RVC.

- Essential Requirements -
The clinical aspect of this project means that only applications from qualified veterinary surgeons will be considered.
Students without English as a first language must provide evidence that they meet the English language requirement.

- Desirable Requirements -
Previous completion of a small animal internal medicine residency would be desirable, but not vital. Please note that residency-trained candidates do not yet need to be board-qualified.

Funding Notes

This is a 3 year fully-funded studentship. The project requires clinical work with diabetic cats examined through the Diabetic Remission Clinic and Hypophysectomy Clinic at the RVC’s Queen Mother Hospital for Animals.

This studentship is open to Home/EU applicants. International students are welcome to apply but must be able to fund the difference between UK/EU and international tuition fees.

The studentship will commence October 2020.

References

1 - Niessen SJM, Forcada Y, Mantis P, Lamb CR, Harrington N, Fowkes R, et al. Studying cat (Felis catus) diabetes: Beware of the acromegalic imposter. PLoS One. 2015;10(5):1–18.
2 - Meijnikman AS, Gerdes VE, Nieuwdorp M, Herrema H. Evaluating causality of gut microbiota in obesity and diabetes in humans. Endocr Rev. 2018;39(2):133–53.
3 - Bell ET, Suchodolski JS, Isaiah A, Fleeman LM, Cook AK, Steiner JM, et al. Faecal microbiota of cats with insulin-treated diabetes mellitus. PLoS One. 2014;9(10).
4 - Kieler IN, Osto M, Hugentobler L, Puetz L, Gilbert MTP, Hansen T, Pedersen O, Reusch CE, Zini E, Lutz TA, Bjørnvad CR. Diabetic cats have decreased gut microbial diversity and a lack of butyrate producing bacteria. Sci Rep. 2019 Mar 18;9(1):4822. doi: 10.1038/s41598-019-41195-0. PubMed PMID: 30886210; PubMed Central PMCID: PMC6423039.

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