Kirti Kaul

TL;DR: Adaptation of the liver ("hepatic mitochondrial flexibility") at early stages of obesity-related insulin resistance, which is subsequently lost in NASH is suggested.

TL;DR: The aim of this paper is to introduce the multiple interconnecting biochemical pathways that have been proposed and tested as key contributors in the development of diabetic retinopathy, namely, increased polyol pathway, activation of protein kinase C (PKC), increased expression of growth factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1).

TL;DR: The types of diabetes and diabetic complications such as impairment of immune system, periodontal disease, retinopathy, nephropathy, somatic and autonomic neuropathy, cardiovascular diseases and diabetic foot are introduced.

TL;DR: Evidence showing a link between circulating and locally produced inflammatory biomarkers, such as cell adhesion molecules, pro-inflammatory cytokines and tumour necrosis factor-alpha, TNF-α with the development and progression of diabetic micro-vascular complications is summarized.

TL;DR: Hepatic insulin resistance originates from lipotoxicity but not from lower mitochondrial capacity, which can even transiently adapt to increased peripheral lipolysis, which is prevented during increased hepatic lipogenesis only if adipose tissue lipid storage capacity is preserved.