Linseed Oil Attenuates Liver Inflammation, Fatty Acid Accumulation, and Lipid Distribution in Periportal and Perivenous Hepatocytes Induced by a High-Carbohydrate Diet in Mice.

We evaluated whether linseed oil (LO) modulates the effects of a high-carbohydrate diet (HCD) on liver inflammation, fatty acid (FA) accumulation, and lipid distribution in periportal and perivenous hepatocytes. The control group (control high-carbohydrate diet [HCD-C]) received an HCD with lard and soybean oil as the lipid source. The L10 and L100 groups received the HCD with 10% and 100% of LO as the lipid source, respectively. The animals were killed by decapitation before (day 0) and after receiving the diets. Liver FA composition, inflammation, and fibrogenesis gene expression were evaluated. Also, the percentage of lipid-occupied area in periportal end perivenous hepatocytes were measured. The L100 group exhibited a higher (P < .05) liver amount of omega-3 polyunsaturated FA (n-3 PUFA) and lower (P < .05) amounts of saturated FA (SFA), monounsaturated FA (MUFA), and omega-6 polyunsaturated FA (n-6 PUFA) compared with L10 or HCD-C mice. On day 56, interleukin 10 and type IV collagen gene expression were significantly upregulated and downregulated, respectively in L100. Also, the L100 group showed lower (P < .05) FA accumulation (i.e., total FA, SFA, MUFA, and n-6 PUFA). Also, L10 and L100 presented lower (P < .05) percentage of high lipid-containing portion in periportal and perivenous hepatocytes. We concluded that LO attenuation of liver inflammation promoted by an HCD is associated with increased liver n-3 PUFA levels, so modulating FA composition, deposition, and distribution in periportal and perivenous hepatocytes.

4-Aminoquinoline compounds from the Spanish flu to COVID-19.

In 1918, quinine was used as one of the unscientifically based treatments against the H1N1 virus during the Spanish flu pandemic. Originally, quinine was extracted from the bark of Chinchona trees by South American natives of the Amazon forest, and it has been used to treat fever since the seventeenth century. The recent COVID-19 pandemic caused by Sars-Cov-2 infection has forced researchers to search for ways to prevent and treat this disease. Based on the antiviral potential of two 4-aminoquinoline compounds derived from quinine, known as chloroquine (CQ) and hydroxychloroquine (HCQ), clinical investigations for treating COVID-19 are being conducted worldwide. However, there are some discrepancies among the clinical trial outcomes.Thus, even after one hundred years of quinine use during the Spanish flu pandemic, the antiviral properties promoted by 4-aminoquinoline compounds remain unclear. The underlying molecular mechanisms by which CQ and HCQ inhibit viral replication open up the possibility of developing novel analogs of these drugs to combat COVID-19 and other viruses.

The Dietary Replacement of Soybean Oil by Canola Oil Does Not Prevent Liver Fatty Acid Accumulation and Liver Inflammation in Mice.

A high-carbohydrate diet (HCD) is a well-established experimental model of accelerated liver fatty acid (FA) deposition and inflammation. In this study, we evaluated whether canola oil can prevent these physiopathological changes. We evaluated hepatic FA accumulation and inflammation in mice fed with a HCD (72.1% carbohydrates) and either canola oil (C group) or soybean oil (S group) as a lipid source for 0, 7, 14, 28, or 56 days. Liver FA compositions were analyzed by gas chromatography. The mRNA expression of acetyl-CoA carboxylase 1 (ACC1) was measured as an indicator of lipogenesis. The mRNA expression of F4/80, tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, and IL-10, as mediators of liver inflammation, were also measured. The C group stored less n-6 polyunsaturated FAs (n-6 PUFAs) and had more intense lipid deposition of monounsaturated FAs (MUFAs), n-3 PUFAs, and total FAs. The C group also showed higher ACC1 expression. Moreover, on day 56, the C group showed higher expressions of the inflammatory genes F4/80, TNF-α, IL-1ß, and IL-6, as well as the anti-inflammatory IL-10. In conclusion, a diet containing canola oil as a lipid source does not prevent the fatty acid accumulation and inflammation induced by a HCD.

Liver Fatty Acid Composition and Inflammation in Mice Fed with High-Carbohydrate Diet or High-Fat Diet.

Both high-carbohydrate diet (HCD) and high-fat diet (HFD) modulate liver fat accumulation and inflammation, however, there is a lack of data on the potential contribution of carbohydrates and lipids separately. For this reason, the changes in liver fatty acid (FA) composition in male Swiss mice fed with HCD or HFD were compared, at the time points 0 (before starting the diets), and after 7, 14, 28 or 56 days. Activities of stearoyl-CoA desaturase-1 (SCD-1), ∆-6 desaturase (D6D), elongases and de novo lipogenesis (DNL) were estimated. Liver mRNA expression of acetyl-CoA carboxylase 1 (ACC1) was evaluated as an additional indicator of the de novo lipogenesis. Myeloperoxidase activity, nitric oxide (NO) production, and mRNA expressions of F4/80, type I collagen, interleukin (IL)-6, IL-1ß, IL-10, and tumor necrosis factor-α (TNF-α) were measured as indication of the liver inflammatory state. The HCD group had more intense lipid deposition, particularly of saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs). This group also showed higher DNL, SCD-1, and D6D activities associated with increased NO concentration, as well as myeloperoxidase activity. Livers from the HFD group showed higher elongase activity, stored more polyunsaturated fatty acids (PUFAs) and had a lower omega-6/omega-3 fatty acid (n-6/n-3) ratio. In conclusion, liver lipid accumulation, fatty acids (FA) composition and inflammation were modulated by the dietary composition of lipids and carbohydrates. The HCD group had more potent lipogenic and inflammatory effects in comparison with HFD.

Oral lactate intensifies insulin toxicity during severe insulin-induced hypoglycemia in mice

ABSTRACT We investigated whether oral lactate could prevent seizures and deaths in mice with severe hypoglycemia induced by a high dose of insulin. For this purpose, mice were fasted for 15 h and then given an intraperitoneal injection of regular insulin (5.0 U/kg or 10.0 U/kg). Immediately after insulin injection, the mice received an oral dose of saline (control), glucose (5.5 mmol/kg), or lactate (18.0 mmol/kg). Glucose and lactate levels were measured in the blood and brain before and after the seizures began. Glucose and lactate delayed (p < 0.05) the onset of seizures associated with severe insulin-induced hypoglycemia. Elevated (p < 0.05) brain levels of lactate were associated with an absence of seizures in mice that received glucose or lactate, suggesting that lactate could prevent convulsions associated with severe insulin-induced hypoglycemia. However, the same oral dose of lactate that delayed the onset of convulsions also increased the mortality rate. In contrast, diazepam (3.0 mg/kg) prevented seizures and markedly decreased the frequency of death during severe insulin-induced hypoglycemia. The results demonstrated that in contrast to oral glucose, oral lactate intensifies insulin toxicity.

Investigation of the Acute Effects of Dry Extract of Glycine Max on Postprandial Glycemia in Rats

The acute effects of Glycine max (GM) on post prandial glycemia (PPG) in male Wistar rats were investigated. All substances were orally administered by gavage in overnight fasted animals. The elevation of PPG promoted by starch (1g/kg) was prevented by GM (2.5 mg/kg, 5.0 mg/kg, 7.5 mg/kg, 10.0 mg/kg, and 100.0 mg/kg). In conclusion GM showed potential antidiabetic effect.