Konjac Glucomannan: An Emerging Specialty Medical Food to Aid in the Treatment of Type 2 Diabetes Mellitus

Abstract

There are many factors causing T2DM; thus, it is difficult to prevent and cure it with conventional treatment. In order to realize the continuous intervention of T2DM, the treatment strategy of combining diet therapy and traditional medication came into being. As a natural product with the concept of being healthy, konjac flour and its derivatives are popular with the public. Its main component, Konjac glucomannan (KGM), can not only be applied as a food additive, which greatly improves the taste and flavor of food and extends the shelf life of food but also occupies an important role in T2DM. KGM can extend gastric emptying time, increase satiety, and promote liver glycogen synthesis, and also has the potential to improve intestinal flora and the metabolic system through a variety of molecular pathways in order to positively regulate oxidative stress and immune inflammation, and protect the liver and kidneys. In order to establish the theoretical justification for the adjunctive treatment of T2DM, we have outlined the physicochemical features of KGM in this article, emphasizing the advantages of KGM as a meal for special medical purposes of T2DM.

Enhancing Metabolic Parameters: The Impact of Porang Glucomannan on Body Weight, Intraperitoneal Fat, Fasting Blood Glucose, and GLUT-4 Levels in Rats Fed a High-Fat and High-Carbohydrate Diet

“…The presence of insoluble fibre and the formation of a thick gel by glucomannan contributed to the delay in gastric emptying, prolonged satiety, and subsequent reduction in body weight among adults with overweight or obese. 7,8 According to the European Food Safety Authority (EFSA), consuming 3 g of glucomannan in divided doses can effectively reduce body weight in overweight adults. Fasting blood glucose (FBG) levels in rats supplemented with porang glucomannan at a dose of 100 mg/200 g BW exhibited a similar trend to the average body weight and was significantly different compared to the normal group.…”

“…16 These findings align with previous research conducted by Fang, who stated that glucomannan reduces blood glucose levels and lowers the risk of diabetes mellitus type 2. 8 Porang glucomannan also has a prebiotic effect. 17 Another research revealed that supplementation with inulin, another prebiotic substance, improved glucose levels, serum insulin, and HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) in rats model of metabolic syndrome.…”

“…It shares a similar soluble fibre structure 7 to konjac glucomannan, which is prevalent in Japan, Korea, and China. 8 Previous research have demonstrated that supplementation with konjac glucomannan at a dosage of 3 g/day has a positive impact on reducing body weight in adults who are overweight or obese. 7,9,10 Glucomannan possesses a structure that resists breakdown by salivary amylase and pancreatic amylase enzymes, making it susceptible to fermentation by bacteria in the colon.…”

“…13 Another research showed that porang glucomannan supplementation increases HDL levels and reduces total cholesterol, triglyceride, and LDL levels in rats with metabolic syndrome. 8 Given the structural similarity between porang glucomannan and konjac glucomannan, it is reasonable to expect that porang glucomannan holds various potential advantages for managing metabolic syndrome. However, research on the specific benefits of porang glucomannan is still limited.…”

Advances in Antioxidant Applications for Combating 131I Side Effects in Thyroid Cancer Treatment

“…This is due to ultrastructural changes resulting in a decreased antioxidant capacity [ 58 , 59 ]. In other words, the levels of enzymatic antioxidants, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and thioredoxin (Trx), as well as non-enzymatic antioxidants such as glutathione (GSH), ascorbic acid, and tocopherol, were reduced in response to 131 I [ 60 , 61 ]. Herein, ferroptosis described a novel form of regulatory cell death that was induced by fatal lipid peroxidation [ 62 ], dependent on iron, which was subsequently induced by an oxidation-damaged phospholipid accumulation and associated with the glutathione-dependent antioxidant defense dysfunction mediated by GPX4 via various pathways.…”