Introduction: Our study aim was to assess how the macronutrient intake during total parenteral nutrition (TPN) modulates plasma total free fatty acids (FFAs) levels and individual fatty acids in critically ill patients. Method: Adult patients aged 18–80, admitted to the intensive care unit (ICU), who were indicated for TPN, with an expected duration of more than three days, were included in the study. Isoenergetic and isonitrogenous TPN solutions were given with a major non-protein energy source, which was glucose (group G) or glucose and lipid emulsions (Smof lipid; group L). Blood samples were collected on days 0, 1, 3, 6, 9, 14, and 28. Results: A significant decrease (p < 0.001) in total FFAs occurred in both groups with a bigger decrease in group G (p < 0.001) from day 0 (0.41 ± 0.19 mmol∙L⁻¹) to day 28 (0.10 ± 0.07 mmol∙L⁻¹). Increased palmitooleic acid and decreased linoleic and docosahexaenoic acids, with a trend of increased mead acid to arachidonic acid ratio, on day 28 were observed in group G in comparison with group L. Group G had an insignificant increase in leptin with no differences in the concentrations of vitamin E, triacylglycerides, and plasminogen activator inhibitor-1. Conclusion: Decreased plasma FFA in critically ill patients who receive TPN may result from increased insulin sensitivity with a better effect in group G, owing to higher insulin and glucose dosing and no lipid emulsions. It is advisable to include a lipid emulsion at the latest from three weeks of TPN to prevent essential fatty acid deficiency.

Multiple non-aggregatory functions of human platelets (PLT) are widely acknowledged, yet their functional examination is limited mainly due to a lack of standardized isolation and analytic methods. Platelet apheresis (PA) is an established clinical method for PLT isolation aiming at the treatment of bleeding diathesis in severe thrombocytopenia. On the other hand, density gradient centrifugation (DC) is an isolation method applied in research for the analysis of the mitochondrial metabolic profile of oxidative phosphorylation (OXPHOS) in PLT obtained from small samples of human blood. We studied PLT obtained from 29 healthy donors by high-resolution respirometry for comparison of PA and DC isolates. ROUTINE respiration and electron transfer capacity of living PLT isolated by PA were significantly higher than in the DC group, whereas plasma membrane permeabilization resulted in a 57% decrease of succinate oxidation in PA compared to DC. These differences were eliminated after washing the PA platelets with phosphate buffer containing 10 mmol·L⁻¹ ethylene glycol-bis (2-aminoethyl ether)-N,N,N′,N′-tetra-acetic acid, suggesting that several components, particularly Ca²⁺ and fuel substrates, were carried over into the respiratory assay from the serum in PA. A simple washing step was sufficient to enable functional mitochondrial analysis in subsamples obtained from PA. The combination of the standard clinical PA isolation procedure with PLT quality control and routine mitochondrial OXPHOS diagnostics meets an acute clinical demand in biomedical research of patients suffering from thrombocytopenia and metabolic diseases.

Carbohydrate (CHO) intake in oral and enteral nutrition is regularly reduced in nutritional support of older patients due to the high prevalence of diabetes (usually type 2—T2DM) in this age group. However, CHO shortage can lead to the lack of building blocks necessary for tissue regeneration and other anabolic processes. Moreover, low CHO intake decreases CHO oxidation and can increase insulin resistance. The aim of our current study was to determine the extent to which an increased intake of a rapidly digestible carbohydrate—maltodextrin—affects blood glucose levels monitored continuously for one week in patients with and without T2DM. Twenty-one patients (14 T2DM and seven without diabetes) were studied for two weeks. During the first week, patients with T2DM received standard diabetic nutrition (250 g CHO per day) and patients without diabetes received a standard diet (350 g of CHO per day). During the second week, the daily CHO intake was increased to 400 in T2DM and 500 g in nondiabetic patients by addition of 150 g maltodextrin divided into three equal doses of 50 g and given immediately after the main meal. Plasma glucose level was monitored continually with the help of a subcutaneous sensor during both weeks. The increased CHO intake led to transient postprandial increase of glucose levels in T2DM patients. This rise was more manifest during the first three days of CHO intake, and then the postprandial peak hyperglycemia was blunted. During the night’s fasting period, the glucose levels were not influenced by maltodextrin. Supplementation of additional CHO did not influence the percentual range of high glucose level and decreased a risk of hypoglycaemia. No change in T2DM treatment was indicated. The results confirm our assumption that increased CHO intake as an alternative to CHO restriction in type 2 diabetic patients during oral and enteral nutritional support is safe.

Background: Since many acutely admitted older adults display signs of dehydration, treatment using balanced crystalloids is an important part of medical care. Additionally, many of these patients suffer from chronic malnutrition. We speculated that the early addition of glucose might ameliorate the hospital-related drop of caloric intake and modify their catabolic status. Methods: We included patients 78 years and older, admitted acutely for non-traumatic illnesses. The patients were randomized into either receiving balanced crystalloid (PlasmaLyte; group P) or balanced crystalloid enriched with 100 g of glucose per liter (group G). The information about fluid balance and levels of minerals were collected longitudinally. Results: In the G group, a significantly higher proportion of patients developed signs of refeeding syndrome, i.e., drops in phosphates, potassium and/or magnesium when compared to group P (83.3 vs. 16.7%, p < 0.01). The drop in phosphate levels was the most pronounced. The urinalysis showed no differences in the levels of these minerals in the urine, suggesting their uptake into the cells. There were no differences in the in-hospital mortality or in the 1-year mortality. Conclusion: The short-term administration of balanced crystalloids with glucose induced an anabolic shift of electrolytes in acutely admitted older adults.

Metformin-associated lactic acidosis (MALA) involves mitochondrial Complex I inhibition, traditionally diagnosed via indirect markers. We present platelet high-resolution respirometry (HRR) as a novel “liquid biopsy” to directly quantify metformin-induced systemic bioenergetic lesions. A 65-year-old diabetic male presented with severe lactic acidosis, acute kidney injury, and profound hypoglycemia after intentionally overdosing on metformin (120 g), dapagliflozin (600 mg), and insulin glargine (300 U). While hemodialysis cleared plasma metformin and resolved the acidosis, refractory hypoglycemia required high-dose IV glucose for over six days. Day 2 platelet HRR revealed severe Complex I inhibition despite significantly decreased plasma metformin, indicating a profound “toxicodynamic lag.” Mitochondrial bioenergetics recovered by Day 7, reflecting natural platelet turnover. The protracted hypoglycemia was driven by a synergistic triad: metformin-inhibited gluconeogenesis, insulin glargine’s prolonged depot effect, and dapagliflozin-induced persistent renal glucose wasting. Platelet HRR has the potential to be a clinically applicable tool to reveal the “hidden” cellular phase of metformin toxicity missed by standard biomarkers. Furthermore, clinicians must anticipate severe, protracted hypoglycemia in mixed overdoses involving SGLT2 inhibitors.

Introduction: Managing glycemic fluctuations in critically ill elderly patients with type 2 diabetes mellitus (T2DM) poses significant challenges. This case report presents a unique scenario in which increased intravenous glucose (Glc) infusion, together with insulin therapy, improved glycemic control and reduced insulin requirements during a septic episode. This finding adds to the scientific literature by suggesting that adequate Glc administration may enhance insulin sensitivity in critically ill T2DM patients. Case report: An 84-year-old female patient with T2DM, hypertension, and chronic renal failure was admitted to the intensive care unit with fever, nausea, loss of appetite, and profound weakness. Laboratory findings revealed severe hyperglycemia, electrolyte imbalances, and markedly elevated inflammatory markers, leading to the diagnosis of decompensated T2DM that was complicated by sepsis. The initial treatment consisted of continuous intravenous (IV) insulin, crystalloid infusions, and broad-spectrum antibiotics. Despite insulin therapy and the absence of nutritional intake, the patient experienced extreme fluctuations in their blood glucose levels, ranging from hyperglycemia to hypoglycemia. Due to persistent glycemic instability, IV Glc infusion was initiated alongside continuous insulin therapy. Paradoxically, increasing Glc infusion administration rate led to a reduction in the required insulin doses and stabilization of blood glucose levels below 10 mmol·L⁻¹. The patient’s C-peptide levels were initially elevated but subsequently decreased following Glc administration as well, suggesting a reduction in endogenous insulin secretion and therefore higher insulin sensitivity. The patient’s clinical condition improved, allowing for the transition to a subcutaneous insulin regime and the initiation of oral feeding. She was later transferred to a general medical ward and discharged without further complications. Conclusions: This case highlights the complex interplay between Glc and insulin in critically ill elderly patients with T2DM during sepsis. The main takeaway is that carefully managed Glc infusion, in conjunction with flexible insulin therapy, can enhance insulin sensitivity and stabilize blood glucose levels without causing further hyperglycemia. Frequent glycemia monitoring and adaptable glycemic management strategies are essential in the ICU to address rapid glycemic fluctuations in this patient population.