The changing notion of “companion animals” and their increasing global status as family members underscores the dynamic interaction between gut microbiota and host health. This review provides a comprehensive understanding of the intricate microbial ecology within companion animals required to maintain overall health and prevent disease. Exploration of specific diseases and syndromes linked to gut microbiome alterations (dysbiosis), such as inflammatory bowel disease, obesity, and neurological conditions like epilepsy, are highlighted. In addition, this review provides an analysis of the various factors that impact the abundance of the gut microbiome like age, breed, habitual diet, and microbe-targeted interventions, such as probiotics. Detection methods including PCR-based algorithms, fluorescence in situ hybridisation, and 16S rRNA gene sequencing are reviewed, along with their limitations and the need for future advancements. Prospects for longitudinal investigations, functional dynamics exploration, and accurate identification of microbial signatures associated with specific health problems offer promising directions for future research. In summary, it is an attempt to provide a deeper insight into the orchestration of multiple microbial species shaping the health of companion animals and possible species-specific differences.

The online version contains supplementary material available at 10.1038/s41598-025-24488-5.

Puberty is a crucial developmental phase influenced by neuroendocrine signals involving various neuropeptides and hormones. The impact of various diet combinations on the initiation of puberty in female rats was studied, along with the crosstalk between hypothalamic neuropeptides that might influence it. Weaned female Wistar rats were segregated into five groups and given different diets for a duration of 21 d. The diet included high-fat, high-carbohydrate, high-protein, cafeteria diet and standard chow. Throughout the 21-day period, body weight, vaginal opening and blood samples were recorded. Post sacrifice parameters like hormonal analysis, gene expression, protein expression and Immunolocalization were performed. The High Fat Diet (HFD), High carbohydrate Diet (HCD), and Cafeteria diet (CafD) groups exhibited early vaginal opening, increased body weight, elevated somatic indices, and Follicle-stimulating Hormone (FSH), Luteinizing Hormone (LH), and estradiol levels were elevated in regards to the control group. Gene expression analysis showed upregulation of Kiss1, Kiss1r, Pomc, Lep, Lepr, and Gnrh, while Npy, Agrp, and Mkrn3 were downregulated. Protein expression studies confirmed the increased levels of KISS1, KISS1R, LEPR, and POMC, particularly in the HFD and HCD groups. Histone acetylation analysis revealed higher global acetylation in the hypothalamus of HFD and HCD groups. This study highlights the significant role of dietary composition in modulating pubertal onset through the neuroendocrine pathways. These findings suggest that high-fat and high-carbohydrate diets expedite puberty by altering the expression of key hypothalamic neuropeptides and hormones. This underscores the importance of nutrition in reproductive development and its broad implications for adolescent health.

This study digs into the complexities of pubertal onset, a critical stage that includes sexual maturation, growth, and the development of secondary sexual features. The highly controlled process involves the Hypothalamic-Pituitary-Gonadal (HPG) axis, which orchestrates pubertal initiation via hormones, neuropeptides, and neurotransmitters such as Kisspeptin. Kisspeptin's involvement in GnRH release and its complex regulation by estrogen, Neuropeptide Y, and miRNAs are investigated. In this intricate network, dysregulation can result in delayed or premature puberty. The work emphasizes the importance of novel detection methods, pointing to early changes in Kisspeptin and GnRH levels, as well as changes in transcriptional component expression patterns, as potential indicators for pubertal start. Because the genetic/familial variables that contribute to pubertal timing are heterogeneous, developing a standard detection method remains difficult, underlining the necessity of multidimensional approaches in understanding and identifying pubertal onset signals.