Obesity and diabetes are the two major metabolic complications linked with bad eating habits and the sedentary (lazy) lifestyle. In the worst-case situation, metabolic problems are a causative factor for numerous other conditions. There is also an increased demand to control the emergence of such diseases. Dietary and lifestyle improvements contribute to their leadership at an elevated level. The present review, therefore, recommends the use of the ketogenic diet (KD) in obesity and diabetes treatment. The KD involves a diet that replaces glucose sugar with ketone bodies and is effective in numerous diseases, such as metabolic disorders, epileptic seizures, autosomal dominant polycystic disease of the kidney, cancers, peripheral neuropathy, and skeletal muscle atrophy. A lot of high profile pathways are available for KD action, including sustaining the metabolic actions on glucose sugar, suppressing insulin-like growth factor-1 (IGF1) and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathways, altering homeostasis of the systemic ketone bodies, contributing to lowering diabetic hyperketonemia, and others. The KD regulates the level of glucose sugar and insulin and can thus claim to be an effective diabetes approach. Genetics1.Peroxisome Proliferator-Activated Receptor-γ2 (PPAR-γ2) Gene that regulates of lipid and glucose homeostasis. 2.Kir6.2 Gene (KCNJ11).3.MODY genes (HNF4aand HNF1β)4.Transcription Factor 7-like(TCF7L2)Gene: helps in the glucose homeostasis. 5.Calpain-10 Gene: Calpains are Ca2+dependent cystein proteases and regulats insulin secretion and action.Mechanisms linking Obesity and DiabetesObesity is a condition associated with multiple medical, social, and psychological problems, the most harmful of which could be T2DM. Both T2DM & obesity have been associated with insulin resistance. KD that connects obesity to diabetes needs to be explained through various mechanisms, the ectopic deposition of lipids may be one of the factors of metabolic syndrome. Most people who are overweight do not experience hyperglycemia besides being insulin resistant. Pancreatic β-cells in the islet of Langerhans release sufficient quantities of insulin to combat its decrease under normal physiological situations, thus retaining normal tolerance to glucose. Normal history of T2DM indicates that endothelial dysfunction is closely linked to obesity /IR in diabetes and pre-diabetic complications. The development of IR and obesity, thus triggering T2DM, cells should possess an inability to respond to impaired insulin sensitivity. Non-esterified fatty acids (NEFAs) discharged from fat-storing tissue in obese individuals can contribute to the theory [38]that IR and β-cell damage are the most important related factors. Thus, a stopgap between obesity and diabetes treatment can also be evidenced by KD.

Pancreatic disorders and Therapy is now accepting submissions on this topic. A standard EDITORIAL TRACKING SYSTEM is utilized for manuscript submission, review, editorial processing and tracking which can be securely accessed by the authors, reviewers and editors for monitoring and tracking the article processing. Manuscripts can be uploaded online at Editorial Tracking System (www.longdom.org/submissions/pancreatic-disorders-therapy.html ) or forwarded to the Editorial Office at manuscripts@longdom.org

Regards,

Jessica Celina

Managing Editor

Pancreatic disorders and Therapy