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Other Complications of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Gastrointestinal complications of diabetes are often caused by abnormal GI motility, a result of diabetic autonomic neuropathy of the GI tract. Factors that contribute to diabetes-related reflux include hyperglycemia, obesity, and decrease bicarbonate secretion from the parotid glands. Gastroparesis is idiopathic in more than 50% of all cases, but autonomic neuropathy remains a significant cause of the condition in people with type 1 or type 2 diabetes. Between 30% and 50% of affected patients have had diabetes for years. The vagus nerve becomes damaged by years of high blood glucose, or insufficient transport of glucose into the cells. Constipation, as part of intestinal enteropathy, is caused by neuronal dysfunction in the large intestine as well as impairment of the gastrocolic reflex. If an individual has elevated hepatic transaminase levels, it is important to assess other possible causes of liver disease, which include hepatitis and hemochromatosis. The cause of nonalcoholic fatty liver disease is unknown but is often related to obesity and type 2 diabetes. All severely obese patients with diabetes have some amount of steatosis, and about 50% have steatohepatitis.
Weight and health
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Non-alcoholic fatty liver disease occurs because of an accumulation of fat in the liver. Not only does this damage the liver, but it is linked to developing type 2 diabetes, high blood pressure and kidney disease.
Metabolic Effects of Exercise on Childhood Obesity
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Kristi B. Adamo, Taniya S. Nagpal, Danilo F. DaSilva
There is a strong relationship between childhood obesity, markers of oxidative stress, and liver diseases. Both oxidative stress and liver disease are moderated by insulin resistance, higher levels of free fatty acids, and visceral fat accumulation. Changes in free fatty acids can trigger increased reactive oxygen species, and thus generate greater oxidative stress responses (73). The increased oxidative stress can result in hepatocyte damage (93). Additionally, excessive abdominal fat increases the risk for non-alcoholic fatty liver disease (54).
Low-intensity exercise diverts cardiac fatty acid metabolism from triacylglycerol synthesis to beta oxidation in fructose-fed rats
Published in Archives of Physiology and Biochemistry, 2023
Milan Kostić, Goran Korićanac, Snežana Tepavčević, Jelena Stanišić, Snježana Romić, Tijana Ćulafić, Tamara Ivković, Mojca Stojiljković
High consumption of fructose may cause problems due to its lipogenic potential (Herman and Samuel 2016). A significant increase in hepatic de novo lipogenesis is one of the major adverse causes for metabolic burden under high fructose consumption. It leads to hepatic lipid accumulation and non-alcoholic fatty liver disease. In addition, increased plasma triacylglycerols (TAG) and very-low-density lipoprotein (VLDL) – TAG levels induce TAG accumulation in extrahepatic tissues, leading to lipotoxicity and insulin resistance in response to high fructose consumption. Fructose-induced lipotoxicity leads to autophagy in skeletal muscle, cardiac dysfunction, adipose tissue inflammation, chronic kidney diseases, pancreatic islet dysfunction, brain oxidative stress and inflammation (reviewed in Zhang et al.2017). This diet is also accompanied by the development of insulin resistance in the heart (Zakula et al.2011, Stanišić et al.2016) and it could change the use of cardiac energy substrates towards increased fatty acid (FA) uptake and catabolism (Coort et al.2007, Zhang et al.2017).
Vitamin E protects against the modulation of TNF-α-AMPK axis and inhibits pancreas injury in a rat model of L-arginine-induced acute necrotising pancreatitis
Published in Archives of Physiology and Biochemistry, 2023
Fahaid Al-Hashem, Mohamed Abd Ellatif, Asmaa M. ShamsEldeen, Samaa S. Kamar, Bahjat Al-Ani, Mohamed A. Haidara
The pleotropic effects of vitamin E is well documented. For example, vitamin E is proposed (i) to treat non-alcoholic fatty liver disease (El Hadi et al. 2018) and liver fibrosis and cirrhosis (Di Sario et al. 2007) via the reduction of oxidative stress; (ii) to reduce inflammation, dyslipidemia and mitochondrial dysfunction in ageing-associated cardiovascular diseases (Ramanathan et al. 2018a); and (iii) to promote cartilage repair by stimulating anabolic metabolism of chondrocytes and/or inhibiting catabolic processes found in osteoarthritis (Altman et al. 1987). In addition, vitamin E lowered the risk of pancreatic cancer in male smokers (Stolzenberg-Solomon 2009). Furthermore, the link between inflammation and adenosine monophosphate-activated protein kinase (AMPK) is well-documentd via the modulation of the trasnscription factor, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), and vitamin E was reported to inhibit constitutive NF-κB activation in pancreatic cancer cells (Husain et al., 2011, Salminen et al. 2011).
Sex disparities and the risk of urolithiasis: a large cross-sectional study
Published in Annals of Medicine, 2022
Jin-Zhou Xu, Cong Li, Qi-Dong Xia, Jun-Lin Lu, Zheng-Ce Wan, Liu Hu, Yong-Man Lv, Xiao-Mei Lei, Wei Guan, Yang Xun, Shao-Gang Wang
Urolithiasis is more prevalent in males compared to females with a prevalence of 9% in females and 19% in males, although the difference is reported to be narrowing [4]. The development of kidney calculi presents obvious sex differences. In addition, both risk factors and consequences of urolithiasis are distinct in different genders [5]. Seolhye et al. manifested that non-alcoholic fatty liver disease is a risk factor for males but not for females [6]. Diabetes mellitus and obesity were also reported to have a stronger association with the risk for urolithiasis in males [7]. Although quite a few studies were devoted to unraveling the relationship between sex and the development of urolithiasis, limitations such as uncontrolled bias, and limited generalisation scope urge more research to facilitate the comprehension of gender differences in urolithiasis.