Spirulina (formerly Arthrospira) maxima (SP) is a cyanobacterium reported to have great nutritional and pharmacological potential. The objective of this study was to evaluate the protective properties of SP against ethanol-induced toxicity. Male Wistar rats were used in the study and subjected to a 70% partial hepatectomy (PH); they were then divided into five groups. During the experiment, animals in two groups drank an aqueous solution of ethanol (EtOH) (40%, v/v). Additionally, they were administered an SP extract daily at a dose of 200 mg/kg body weight intragastrically. To explore possible mechanisms of action, we examined antioxidant defense enzymes, as well as serum biochemical parameters and histopathological changes in the liver. SP administration normalized elevated glutathione reductase (GR), glutathione (GSH), and superoxide dismutase (SOD) levels, in addition to increased catalase (CAT) and glutathione peroxidase (GPX) enzymes. Alterations in biochemical parameters were observed in the groups with PH treated with EtOH associated with a reduction in cholesterol and albumin levels, while glucose and triglyceride levels increased. The histological study supported the protective activity of SP, reducing apoptosis, necrosis, and congestion in the liver. Our findings demonstrated a protective effect of SP against EtOH that is related to less inflammation, a lesser antioxidant effect, and less free radical scavenging activity.

High-density lipoprotein cholesterol (HDL-C) is reported as a biomarker of systemic inflammation and multi-organ failure (MOF), which has been rarely investigated in acute pancreatitis (AP), a frequent condition in the emergency department (ED). The objective was to study the predictive capacity of the decrease in HDL-C to the progression of MOF in AP in the ED; analyzing 114 patients with AP for one year in a longitudinal and prospective study, AP severity was obtained by the Atlanta classification, in relation to modified Marshall and Bedside Index for Severity in Acute Pancreatitis (BISAP) scores, and clinical and laboratory parameters in a 48 h hospital stay. The area under the receiver operating characteristic (ROC) curve was used to estimate the validity of the predictor and define optimal cut-off points. It was found that AP was classified as severe in 24.5%, mainly for biliary etiology (78.9%) and female sex (73.6%). As a biomarker, HDL-C decreased from 31.6 to 29.5 mg/dL in a 48 h stay (p < 0.001), correlating negatively with the increase in severity index > 2 and the modified Marshall (p < 0.032) and BISAP (p < 0.009) scores, finding an area under the ROC curve with a predictive capacity of 0.756 (95% CI, 0.614–0.898; p < 0.004) and a cut-off point of 28.5 mg/dL (sensitivity: 79%, specificity: 78%), demonstrating that the decrease in HDL-C levels serves as a useful indicator with a predictive capacity for MOF in mild to severe AP, during a 48 h hospital stay in the ED.

Hyperlipidemia due to a high-fat diet (HFD) is a risk factor for inducing insulin resistance (IR) and adverse effects on pancreatic β-cells in obesity and type 2 diabetes mellitus. This relationship may be due to activation of the hexosaminebiosynthesis pathway. Administration of exogenous glucosamine (GlcN) can increase the end product of this pathway (uridine-5′-diphosphate-N-acetyl-glucosamine), which can mediate IR and protein glycosylation. The objective of this study was to evaluate the effects of oral GlcN and HFD on IR and pancreatic histologic damage in a 22 wk study of 4 groups of male Wistar rats: control group with normal chow diet, HFD group (24%. g/g lard), GlcN group (500 mg/kg^–1 per day of glucosamine hydrochloride in drinking water) and HFD plus oral GlcN. Metabolic variables related to IR that were measured included triglycerides (TG), free fatty acids (FFAs) and malondialdehyde (MDA). Histopathologic evaluation of the pancreas was also performed. The results showed IR in the HFD group, which had increased pancreatic nuclear pyknosis and vacuolization, with fatty infiltration and structural alteration of the islets of Langerhans. TG, FFAs and MDA were higher in serum and pancreatic tissue as compared with the control group. The GlcN group did not develop IR and had only mild nuclear pyknosis with no significant change in the pancreatic content of TG, FFAs and MDA. However, the combined administration of GlcN and HFD attenuated IR and improved TG, FFAs and MDA levels in serum and pancreatic tissue and the pancreatic histopathologic changes, with no significant differences as compared with the control group. These findings suggest that the oral GlcN at a dose of 500 mg/kg^–1 is protective against IR and the pancreatic histologic damage caused by HFD.

Diabetes mellitus (DM) is a metabolic disorder whose prevalence has continuously increased worldwide and is associated with dysfunction of the autonomic nervous system and, in particular, that of the sympathetic nervous system (SNS). The objective of this study was to analyze the interaction of DM and the SNS, building a model of sympathectomized diabetic rats to determine alterations in the content of CA (catecholamines) in different intra-abdominal organs. Sympathectomy was conducted with guanethidine (GNT). Additionally, DM was induced with STZ (Streptozotocin). Treatment with GNT decreased norepinephrine (NE) content in all analyzed tissues, with significant differences found in the paraganglia, liver, pancreas, duodenum, and heart compared to the control group. With respect to epinephrine (E), which was only found in the liver, pancreas, and heart, presenting significant differences (p < 0.05) in the heart, a decrease in its concentration was observed for all of the experimental groups with respect to the control. The decrease in dopamine (DA) content due to the GNT–STZ treatment was 30.1% in the heart with respect to the diabetic (STZ) group. The amount of CA in the adrenal medulla indicates the effect of sympathectomy on the GNT group where there was a significant reduction (p < 0.05) of DA. These findings suggest that the elimination of the sympathetic nervous system in diabetic organisms contributed to a decrease in blood glucose; likewise, an alteration in the levels of CA was observed in the different selected organs, possibly attributed to the severity, duration, and pathogenesis of the complications of acute and chronic DM.

Although it is desirable to replace scientific procedures with live animals by other methods that do not use them, the use of animals in scientific procedures should be restricted to those areas that benefit human, animal, and environmental health. The use of animals as experimental models of observation of biological phenomena has evolved with man, to this day. The use of animals for scientific or educational purposes should be considered only when there is no other alternative and it is governed by the principles of replacement, reduction, and refinement. The scientists should be sure that the information obtainable with the experiments is not yet available or that the protocol was designed taking into account animal protection considerations. The chosen methods must use the least number of animals; provide satisfactory results; use the species with the least ability to experience pain, suffering, anguish, and damage; and be optimal for the extrapolation of results to the target species such as humans. It will be fundamental to guarantee on a scientific and ethical basis that the use of an animal is subject to a careful evaluation regarding the scientific or educational validity.