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Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Metabolic syndrome is linked to nonalcoholic fatty liver disease as well as nonalcoholic steatohepatitis. Nonalcoholic fatty liver disease (NAFLD) is the primary hepatic manifestation of metabolic syndrome. It is one the most common liver disease, and is estimated (in the United States) to be present in 38% of obese children, 34% of adults, and 9.6% of nonobese children. Ultrasound studies show that up to 78% of type 2 diabetes patients have a fatty liver. There is accumulation of triglycerides and various amounts of liver injury, inflammation, and repair. Appearance of this condition mostly depends on increased fatty acid flow from excessive lipolysis from insulin-resistant adipose tissue. About 90% of patients with NAFLD have more than one feature of metabolic syndrome, and about 33% have three or more criteria. Lipotoxicity results in accumulation of triglycerides in the liver, because of imbalances between uptake, synthesis, export, and oxidation of fatty acids. The presence of NAFLD is seen in more than 66% of obese patients. Hepatitis C virus (HCV) infection is more common along with type 2 diabetes, and often coexists along with NAFLD. Hepatic steatosis exists in 50% of people infected with HCV. Combined steatosis with HCV infection leads to more fibrosis and a higher likelihood of the patient not responding to antiviral therapies.
Beta Cells and Diabetes
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Shivani Srivastava, Durgavati Yadav, Kumar Sandeep, Harsh Pandey, Surya Kumar Singh, Yamini Bhusan Tripathi
Diabetes is generally considered a very complex disease. Because of having no clear idea of it, the permanent solution is absent. Even discrimination between Type 1 and Type 2 is also very difficult. Type 1 diabetes is the severe condition of diabetes mellitus (DM) but sometimes it mimics type 2 DM by performing insulin resistance. Mechanism of action involves hyperglycemia/glucotoxicity, lipotoxicity, autoimmunity, inflammation, adipokines, islet amyloid, incretins, and insulin resistance in DM (Cernea and Dobreanu, 2013). Insulin gets released from pancreatic β cells when circulating blood glucose reaches a threshold. Insulin performs two major functions: first, it stores glucose in skeletal muscles and liver in the form of glycogen and simultaneously inhibits glucose secretion from the liver and second, insulin preserves excess fatty acid in adipose tissue as triglyceride to be used as a reserve for energy release, in case of fasting. Excess intake of free fatty acids (FFAs), lack of exercise, glucocorticoid administration, and obesity are the main inducers of insulin resistance. In pathological conditions like obesity, these fatty acids get accumulated in the muscle, liver, and β cells, thus creating lipotoxicity. This ectopic accumulation results in insulin resistance and a loss of mass and function of β cells. Altogether, these conditions lead to hyperglycemia and type 2 diabetes (T2D) (Hajduch and Bourron, 2013) (Figure 12.1).
Bamboo as Food and Medicine
Published in Nirmala Chongtham, Madho Singh Bisht, Bamboo Shoot, 2020
Nirmala Chongtham, Madho Singh Bisht
Lipotoxicity is closely associated with the etiology and complications of type 2 diabetes mellitus. An ethanol/water bamboo extract (BEX) of Phyllostachys edulis demonstrated a potent anti-lipotoxicity function in mice thereby relieving the symptoms of type 2 diabetes (Panee 2009). They investigated the protective effect of an extract from Phyllostachys edulis against palmitic acid–induced lipoapoptosis. The lipid detoxification function of the bamboo extract was evaluated using cell culture models. A novel function of bamboo extract that prevented lipotoxicity in mammalian cells was demonstrated implicating a promising phytotherapeutic approach for lipo-detoxification. Subsequent in-vivo studies revealed that BEX significantly improved glucose tolerance, inhibited hyperinsulinemia, lowered hepatic fat content and decreased circulating levels of tumour necrosis alpha (a major pro-inflammatory cytokins) in obese C57BL/6J mice (Koide et al. 2011). These results indicate that BEX inhibits obesity associated with chronic systemic inflammation and ameliorates the symptoms of type 2 diabetes, suggesting a potential application of this natural product as an anti-diabetic nutraceutical.
The role of resveratrol in diabetes and obesity associated with insulin resistance
Published in Archives of Physiology and Biochemistry, 2023
Mustafa Hoca, Eda Becer, Hafize Seda Vatansever
A high-fat diet leads to lipotoxicity, which is described as lipid accumulation in peripheral tissues. This condition is a risk factor for type 2 diabetes development. Functionality loss of β-cells and cellular apoptosis in pancreas are characteristic properties in lipotoxicity-related type 2 diabetes (Yang et al. 2016). Recently, experimental studies using pancreatic β-cells isolated from animal models have suggested that whole pancreatic tissue triglyceride content was reduced by resveratrol. Moreover, this is related to the beneficial effects of resveratrol on silent information regulator 1 (SIRT1) expression and decreases in uncoupling protein-2 (UCP-2) expression in pancreatic beta cells of male C57BL/6J mice (Zhang et al. 2012). UCP-2 is a mitochondrial transporter protein which dissipates metabolic energy with preventing of oxidative stress accumulation and also negatively modulates insulin secretion from pancreas (Chan et al.2004). On the other hand, UCP-2 up-regulation is a stress conditions marker and was observed in some diet-induced β-cell dysfunction animal models. Resveratrol decreased UCP-2 expression in β-cells and improved pancreas functions (Zhang et al.2012). Furthermore, SIRT1 stimulates insulin secretion from pancreas (Bordone et al.2006). The data showed that resveratrol protected and improved β-cells’ functions by reducing oxidative stress.
COVID-19 and hyperglycaemic emergencies: perspectives from a developing country
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2022
Raisa Bhikoo, Marli Conradie-Smit, Gerhard Van Wyk, Sa’ad Lahri, Elizabeth Du Plessis, Jaco Cilliers, Susan Hugo, Ankia Coetzee
From a pathophysiologic perspective, DKA occurs in the presence of relative or absolute insulin deficiency coupled with increased counterregulatory hormones, driving gluconeogenesis, lipolysis and ketogenesis.20 Whilst DKA is characteristically associated with Type 1 DM it is well documented in patients with Type 2 DM, which may also include individuals with the so-called ‘ketosis-prone diabetes’ (KPT2D). Individuals with KPT2D who present in DKA, but phenotypically resemble Type 2 DM, are characteristically overweight or moderately obese and lack autoimmune antibodies associated with Type 1 DM.21 It has been postulated that the increased insulin resistance and decreased insulin secretion are the result of lipotoxicity.22 As opposed to Type 1 DM, pancreatic beta cell function may recover after achieving normoglycemia with insulin therapy in KPT2D, allowing some individuals to become insulin independent.21,22
Cadmium exposure induces cardiac glucometabolic dysregulation and lipid accumulation independent of pyruvate dehydrogenase activity
Published in Annals of Medicine, 2021
Olufemi I. Oluranti, Ebunoluwa A. Agboola, Nteimam E. Fubara, Mercy O. Ajayi, Olugbenga S. Michael
Lipotoxicity is characterized as the accumulation in tissues and organs of lipid intermediates and final products in which it normally does not accumulate. It is thought that lipotoxicity plays a major role in heart disease, obesity and diabetes [10]. Excess lipid accumulation in the heart called cardiac lipotoxicity can cause alterations in the cell as lipids are crucial regulators of the heart function through their role in the structure of the membrane, transport, signalling and β-oxidation substrate for mitochondrial energy production [11,12]. Together with excessive accumulation of intra-myocellular triglycerides (TG), cardiac lipotoxicity often includes changes in various lipid groups and their fatty acid composition, thus, aiding the development of active lipid mediators that influence metabolism and cardiac function, partly by distorting mitochondrial function [13–15].