The impact of weight loss on renal function in individuals with obesity and type 2 diabetes: a comprehensive review

Abstract

Obesity and Type 2 Diabetes (T2D) are two highly prevalent diseases that exhibit a complex interplay between them. Obesity serves as a primary risk factor for the development of T2D, and conversely, individuals with T2D often exhibit comorbid obesity. Renal dysfunction emerges as a critical consequence of the convergence of obesity and Type 2 Diabetes, contributing significantly to the overall burden of complications associated with these conditions. Recognizing the profound implications of renal dysfunction in individuals contending with both obesity and Type 2 Diabetes, interventions targeting weight loss have gained prominence as potential therapeutic avenues. Weight loss not only addresses the primary risk factor of obesity but also holds the promise of mitigating the progression of Type 2 Diabetes and its associated renal complications. This comprehensive review aims to explore the impact of weight loss on renal function in individuals contending with the convergence of obesity and T2D.

Keywords: chronic kidney disease; obesity; renal function; type 2 diabetes; weight loss.

Figure 1

Potential Mechanisms of Weight Loss Intervention in Preserving Renal Function in Obesity and Diabetic Patients. All three approaches—lifestyle modifications, anti-obesity medications, and metabolic surgeries—result in a reduction in patient body weight. This reduction is characterized by a decrease in fat deposition, encompassing visceral fat, renal sinus fat, and ectopic adipose tissue. The reduction of fat in these specific regions promotes the restoration of insulin sensitivity, elevation of peripheral insulin levels, suppression of pro-inflammatory factors, and modulation of adipokine release. Simultaneously, alterations in the release patterns of adipokines are observed, marked by an increase in adiponectin levels and a decrease in leptin levels. Furthermore, the renin-angiotensin-aldosterone system (RAS) is inhibited. Additionally, shifts in gut microbiota composition and increased secretion of hormones such as GLP-1 and PYY contribute to these effects. Collectively, these changes culminate in enhanced regulation of blood glucose, blood lipids, and blood pressure. The inhibition of the RAS system also leads to reduced urinary sodium retention, providing a safeguard for the kidneys. These interventions exert a favorable impact on renal function, including the amelioration of glomerular hyperfiltration, preservation of renal cell integrity, and reduction in renal inflammation. Ultimately, these mechanisms translate into enhancements in kidney structure, including the attenuation of glomerular and renal tubular atrophy, as well as a reduction in interstitial fibrosis. GLP-1(Glucagon-Like Peptide-1); PYY(Peptide YY). Red arrows represent an increase, and blue arrows represent a decrease.