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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.
Nanocarriers Systems and Their Application for the Delivery of Different Phytoconstituents
Published in Madhu Gupta, Durgesh Nandini Chauhan, Vikas Sharma, Nagendra Singh Chauhan, Novel Drug Delivery Systems for Phytoconstituents, 2020
Ebru Altuntaş, Gülgün Yener, Burcu Özkan
The bioavailability of silybin-phospholipid complex was investigated in comparison with silybin-N-methylglucamine. Consequently, extended plasma therapeutic level (Tmax of the phospholipid complex: 10 min; Tmax of silybin-N-methylglucamine: 5 min) and enhanced bioavailability (Cmax of the phospholipid complex: 126.72 ng/mL; Cmax of silybin-N-methylglucamine: 104.29 ng/mL) was obtained with the phospholipid complex (Yanyu et al., 2006). A research of vitamin E combined silybin phosphatidylcholine (Realsil) on 138 patients who have nonalcoholic fatty liver disorder was carried out over 12 months (Loguercio et al., 2012). Normalized aspartate aminotransferase levels were obtained in 43% of patients with realsil and 15% with the placebo. Remarkable developments were determined in the levels of alanine aminotransferase and gamma glutamyltranspeptidase with realsil, while small changes were obtained with the placebo. The results of this research showed that treating the nonalcoholic fatty liver disease successfully, in which no drug has been approved to date, is possible.
Role of Nutraceuticals in Prevention of Nonalcoholic Fatty Liver
Published in Megh R. Goyal, Durgesh Nandini Chauhan, Plant- and Marine-Based Phytochemicals for Human Health, 2018
NAFLD represents the hepatic component of metabolic syndrome. Accu- mulation of fat itself in the liver is not dangerous, but the hazards reside in its progression to steatohepatitis, which is inflammation with fat depo- sition. Different factors of such progression have been proposed, insulin resistance remains to be the most important factor. Steatohepatitis may lead to hepatic cirrhosis and carcinoma and to cardiovascular diseases. Diets and body weight play a major role in both the induction and manage- ment of NAFLD. So far, no established treatment for NAFLD is present except for modifying risk factors such as components of the metabolic syndrome. Nutraceuticals together with low-calorie foods might be an effective approach to control metabolic syndrome aspects including fatty liver. This chapter reviewed different studied nutraceuticals that could have therapeutic efficiency and/or protective effect toward nonalcoholic fatty liver.
Hepatic manifestations of COVID-19 and effect of remdesivir on liver function in patients with COVID-19 illness
Published in Baylor University Medical Center Proceedings, 2021
Abdul Aleem, Guruprasad Mahadevaiah, Nasir Shariff, Jiten P. Kothadia
Liver dysfunction has been reported in patients with severe bacterial sepsis.13 The hemodynamic compromise and severe systemic inflammation could contribute to the abnormal liver function noted in patients with severe COVID-19 infection. With the presence of other comorbid illnesses contributing to a higher risk of hospitalization, underlying metabolic syndrome and underrecognized nonalcoholic fatty liver disease could also be contributory factors. Also, COVID-19 patients with preexisting liver diseases are at a higher risk for decompensation and mortality based on the results of a US-based multicenter study that reported a mortality rate of 12% in COVID-19 patients with preexisting liver disease compared to 4% in those without.14 Various drugs (remdesivir, tocilizumab, acetaminophen, lopinavir-ritonavir, azithromycin, ivermectin) used in the management of COVID-19 are potential hepatoxic drugs, thus implying drug-induced liver injury in the pathogenesis. Notably, in a prospective multicenter study of liver transplant recipients, COVID-19 was associated with an overall and in-hospital fatality rate of 12% (95% CI 5%–24%) and 17% (95% CI 7%–32%), respectively.15
Alcohol and melatonin
Published in Chronobiology International, 2021
Alcohol as an organic solvent can damage cell membranes and mitochondria in liver tissue. Researchers suggest that a prolonged high concentration of acetaldehyde in liver tissue and associated high NADH level are the leading factors of alcoholic fatty liver dystrophy, i.e., a pathological condition caused by disrupted lipid metabolism in hepatocytes leading to fat accumulation in the liver. This intensifies peripheral lipolysis and increases liver uptake of fatty acids (Hatzis et al. 2013). Exposure to acetaldehyde increases the synthesis of triglycerides in liver mitochondria and decreases beta-oxidation of fatty acids and formation of lipoproteins and their escape from the liver (Sookoian and Pirola 2013). An increase in the number and size of fatty inclusions in the hepatocyte leads to a fatal disturbance of hepatic cell metabolism and cellular death, i.e., steatonecrosis (Martínez Soriano et al. 2020). In a study of the liver of non-alcohol abusers conducted in 1980, Ludwig. et al. found a histological picture identical to that of alcoholic hepatitis (Ludwig et al. 1980). The dynamics of this etiological type of liver pathology, termed “nonalcoholic fatty liver disease”, is similar to the alcoholic one: fatty liver dystrophy (nonalcoholic steatosis) – nonalcoholic steatohepatitis – liver cirrhosis (Kotronen et al. 2010; Pan et al. 2006). The criteria for the diagnosis of nonalcoholic fatty liver disease include fatty liver dystrophy or inflammatory changes similar to alcoholic hepatitis in the absence of hepatotoxic alcohol consumption and in the absence of other liver pathology (Abdelmalek 2021; Shao et al. 2020).
Persistent lactic acidosis in the Mauriac syndrome in type 1 diabetes mellitus
Published in Baylor University Medical Center Proceedings, 2021
Abinash Subedi, Vishnu Charan Suresh Kumar, Anuj Sharma, Gilles Hoilat, Savio John
Other causes of hepatomegaly need to be ruled out before Mauriac syndrome is diagnosed. These include infectious, autoimmune, and metabolic (primary glycogen storage diseases) etiologies. Nonalcoholic fatty liver disease is more common in patients with diabetes mellitus type 2. A noncontrast CT scan of the abdomen can differentiate between the two; nonalcoholic fatty liver disease would be seen as a hypodense liver while glycogenic hepatopathy would be seen as a hyperdense liver. Nonalcoholic fatty liver disease is associated with hyperinsulinemia and insulin resistance, whereas glycogenic hepatopathy is associated with insulin deficiency.11 The gold standard test for diagnosis of glycogenic hepatopathy is liver biopsy and demonstration of glycogen accumulation in hepatocytes.12