Mini Review - (2023) Volume 14, Issue 12
Feline diabetes mellitus (DM) is a complex and increasingly prevalent metabolic disorder that shares similarities with human diabetes. This review aims to elucidate the pathophysiological continuum encompassing prediabetes, diabetes, and the intricacies of diabetic remission in felines. The etiological factors contributing to feline diabetes, including genetic predisposition and environmental influences, are explored. The pathophysiology involves disruptions in insulin secretion, insulin action, and glucose metabolism, leading to chronic hyperglycemia. Feline prediabetes, often underdiagnosed, is characterized by early metabolic abnormalities preceding overt diabetes. Understanding the transition from prediabetes to diabetes and the factors influencing diabetic remission is crucial for effective clinical management. This review provides a comprehensive examination of the molecular and physiological events involved in feline diabetes, offering insights into potential therapeutic targets and preventive strategies for this prevalent feline health concern.
Feline diabetes; Prediabetes; Insulin dysfunction; Glucose metabolism; Diabetic remission; Genetic predisposition
Feline diabetes mellitus (DM) poses a significant health concern in the feline population [1], sharing similarities with its human counterpart. This introduction provides an overview of the pathophysiological continuum spanning prediabetes, diabetes, and the intricacies of diabetic reduction in felines. As an intricate interplay of genetic and environmental factors influences the development of diabetes in cats, understanding the underlying pathophysiology is paramount for effective clinical management and preventive measures. The prevalence of feline diabetes has been on the rise, necessitating a comprehensive exploration of its pathophysiology. As feline diabetes closely mirrors human diabetes, studying the feline model offers insights with implications for both veterinary and human medicine. Genetic predisposition and environmental influences contribute to the etiology of feline diabetes. Certain breeds may demonstrate an increased susceptibility, and factors such as diet and lifestyle play pivotal roles [2-4]. Understanding these factors is crucial for tailoring interventions and preventive strategies.
The pathophysiology of feline diabetes involves disruptions in insulin secretion, insulin action, and glucose metabolism. Chronic hyperglycemia ensues, leading to clinical manifestations. This continuum extends to prediabetes, a state characterized by early metabolic abnormalities that precede overt diabetes. Recognizing and understanding prediabetes is vital for timely intervention and prevention. Diabetic remission, wherein cats experience a reduction or normalization of blood glucose levels, is an intriguing aspect of feline diabetes. The factors influencing this phenomenon, including potential reversibility of pancreatic dysfunction, are of clinical significance. Exploring the mechanisms of diabetic reduction offers insights into therapeutic possibilities.
This review aims to comprehensively examine the pathophysiology of feline diabetes, from the molecular events influencing its onset to the complexities of prediabetes and the intriguing aspects of diabetic reduction. By addressing gaps in current understanding, we aim to contribute to the development of targeted interventions and preventive measures for feline diabetes. The discussions on feline diabetes pathophysiology have direct clinical implications, guiding veterinarians in diagnosis, management, and potential avenues for therapeutic interventions [5]. The insights gained may inform personalized approaches to feline diabetes care, optimizing outcomes for affected cats. In summary, this introduction sets the stage for an indepth exploration of the pathophysiology of feline diabetes, emphasizing the continuum from prediabetes to diabetes and the complexities of diabetic reduction. By unraveling these intricacies, we aim to enhance our understanding of feline diabetes and contribute to advancements in clinical practice and veterinary research.
A systematic review of the existing literature on feline diabetes mellitus and related pathophysiology was conducted. Electronic databases such as PubMed, veterinary journals, and relevant conference proceedings were searched for articles published within the last decade. Inclusion criteria encompassed studies focusing on the pathophysiology of feline diabetes, prediabetes, and diabetic reduction [6-8]. Articles providing insights into genetic factors, environmental influences, molecular events, and physiological changes associated with feline diabetes were prioritized.
Pertinent data related to the pathophysiology of feline diabetes, including insulin secretion, insulin action, glucose metabolism, and the transition from prediabetes to diabetes, were systematically extracted. Special attention was given to studies that explored the mechanisms underlying diabetic reduction in felines. Extracted data were synthesized to create a cohesive narrative that addresses the continuum of pathophysiological events in feline diabetes. Connections between genetic predisposition, environmental influences, molecular events, and the clinical manifestations of prediabetes and diabetes were explored. The collected information underwent critical analysis to assess the quality, reliability, and relevance of the sources. Conflicting data or controversial findings were carefully examined, and efforts were made to present a balanced and evidence-based perspective. Special emphasis was placed on understanding the mechanisms underlying diabetic reduction in felines. Studies elucidating factors influencing reversibility of pancreatic dysfunction, hormonal changes, and potential therapeutic targets for diabetic reduction were critically analyzed.
As this study involved a review of existing literature, ethical approval was not required. However, ethical considerations were maintained in ensuring accurate representation of data and proper citation of sources. Acknowledgment of potential limitations, such as variations in study designs and limited availability of specific data on feline prediabetes and diabetic reduction, was included. Efforts were made to mitigate these limitations through a systematic and rigorous review process. By employing these methods, this review aspires to provide a comprehensive understanding of the pathophysiology of feline diabetes, prediabetes, and diabetic reduction, offering insights that contribute to both clinical practice and future research in veterinary medicine.
The literature review revealed evidence supporting a genetic predisposition to feline diabetes, with certain breeds exhibiting higher susceptibility. Environmental factors, including diet and obesity, were identified as significant contributors to the development of diabetes. The interplay between genetic and environmental influences underscores the complexity of feline diabetes pathophysiology. Disruptions in insulin secretion and action were identified as key components of feline diabetes pathophysiology. Impaired beta-cell function and insulin resistance contribute to chronic hyperglycemia. Understanding the molecular events influencing insulin dynamics is crucial for developing targeted interventions.
Alterations in glucose metabolism play a central role in feline diabetes. The review highlighted dysregulation in glucose homeostasis, with impaired uptake by peripheral tissues contributing to elevated blood glucose levels. Insights into these metabolic changes provide a foundation for therapeutic strategies. The continuum from prediabetes to diabetes was explored, emphasizing the importance of recognizing early metabolic abnormalities. Feline prediabetes, often underdiagnosed, represents a critical stage for intervention. Identifying markers of prediabetes and understanding its progression provide opportunities for preventive measures [9]. Diabetic remission in felines emerged as a fascinating aspect of pathophysiology. Factors influencing diabetic reduction, including potential reversibility of pancreatic dysfunction, hormonal changes, and the role of weight loss, were discussed. These insights offer potential therapeutic avenues for managing feline diabetes.
The discussions on feline diabetes pathophysiology have direct clinical implications for veterinarians. Understanding the molecular and physiological events influencing insulin dynamics, glucose metabolism, and the transition from prediabetes to diabetes informs personalized approaches to feline diabetes care. Additionally, insights into diabetic reduction mechanisms may guide therapeutic interventions. Challenges in studying feline diabetes pathophysiology, including variations in study designs and limited availability of specific data on feline prediabetes and diabetic reduction, were acknowledged. The discussions emphasized the need for further research, collaborative efforts, and standardized methodologies to advance our understanding of this complex feline health concern.
In conclusion, the results and discussions provide a comprehensive overview of the pathophysiology of feline diabetes, spanning from genetic predisposition and environmental influences to disruptions in insulin secretion, glucose metabolism, and the intriguing aspects of prediabetes and diabetic reduction [10]. By unraveling these intricacies, this review aims to enhance our understanding of feline diabetes, contributing to advancements in clinical practice and veterinary research. The insights gained may inform targeted interventions, preventive strategies, and potential translational applications for both veterinary and human medicine.
In summary, the exploration of the pathophysiology of feline diabetes, prediabetes, and diabetic reduction provides a nuanced understanding of this complex metabolic disorder. The interplay of genetic predisposition and environmental influences, disruptions in insulin secretion and action, alterations in glucose metabolism, and the continuum from prediabetes to diabetes were comprehensively examined. Additionally, the intriguing aspects of diabetic reduction, including potential reversibility of pancreatic dysfunction, hormonal changes, and the role of weight loss, were discussed. The results underscore the importance of recognizing early metabolic abnormalities in feline prediabetes, a stage often underdiagnosed but critical for intervention. Identifying genetic markers, understanding insulin dynamics, and exploring the factors influencing diabetic reduction offer valuable insights with direct clinical implications. Veterinarians can utilize this knowledge to tailor personalized approaches to feline diabetes care, optimizing outcomes for affected cats.
Challenges in studying feline diabetes pathophysiology were acknowledged, emphasizing the need for further research, collaborative efforts, and standardized methodologies. Addressing these challenges will contribute to a more comprehensive understanding of feline diabetes and open avenues for targeted interventions and preventive measures. In conclusion, this review serves as a stepping stone toward a deeper comprehension of the pathophysiology of feline diabetes. By synthesizing current knowledge, addressing gaps in understanding, and offering potential directions for future research, this work contributes to the ongoing efforts to enhance the clinical management and overall well-being of cats affected by this prevalent metabolic disorder.
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Citation: Ruth Costello. Pathophysiology of Prediabetes, Diabetes, and Diabetic Reduction in Felines. J Diabetes Metab, 2023, 14(12): 1072.
Received: 02-Dec-2023, Manuscript No. jdm-24-28609; Editor assigned: 04-Dec-2023, Pre QC No. jdm-24-28609 (PQ); Reviewed: 18-Dec-2023, QC No. jdm-24-28609; Revised: 23-Dec-2023, Manuscript No. jdm-24-28609 (R); Published: 29-Dec-2023, DOI: 10.35248/2155-6156.10001072
Copyright: © 2023 Costello R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
