Caloric Overfeeding Research Articles

Impact of Propofol Sedation upon Caloric Overfeeding and Protein Inadequacy in Critically Ill Patients Receiving Nutrition Support.

Propofol, a commonly used sedative in the intensive care unit, is formulated in a 10% lipid emulsion that contributes 1.1 kcals per mL. As a result, propofol can significantly contribute to caloric intake and can potentially result in complications of overfeeding for patients who receive concurrent enteral or parenteral nutrition therapy. In order to avoid potential overfeeding, some clinicians have empirically decreased the infusion rate of the nutrition therapy, which also may have detrimental effects since protein intake may be inadequate. The purpose of this review is to examine the current literature regarding these issues and provide some practical suggestions on how to restrict caloric intake to avoid overfeeding and simultaneously enhance protein intake for patients who receive either parenteral or enteral nutrition for those patients receiving concurrent propofol therapy.

Improvement in Protein Delivery for Critically Ill Patients Requiring High-Dose Propofol Therapy and Enteral Nutrition.

Patients with traumatic brain (TBI) injury often require a high dosage of propofol, which can provide an excessive caloric intake. We evaluated our strategy of using liquid protein supplement boluses concurrently with high protein-containing enteral nutrition (EN) formulas and formula rate reduction to avoid caloric overfeeding and inadequate protein intake. Adult patients (aged >17 years) with TBI admitted to the trauma intensive care unit (TICU) who received concurrent propofol and EN were retrospectively reviewed. Caloric intakes from propofol and EN were obtained. Actual protein intake was compared with projected protein intakes from high protein content and standard protein content enteral formulas when given at an isocaloric intake. Fifty-one patients were enrolled. Average caloric intake from propofol was 356 ± 243 kcal/d or 5 ± 3 kcal/kg/d (range, <1-15 kcal/kg/d). Daily EN caloric intake ranged from 7 ± 4 kcal/kg/d (day 2) to 16 ± 9 kcal/kg/d (day 5; P < .001). Average protein intake ranged from 0.6 ± 0.4 g/kg/d (day 2) to 1.5 ± 0.7 g/kg/d (day 5; P < .001). The modified EN strategy resulted in daily delivery of 24%-38% more protein than an isocaloric regimen with a high protein-content formula and twice as much protein than the standard protein-content formula (P < .001). The strategy of providing an EN regimen comprised liquid protein boluses, and high and very high protein-containing EN formulas at a reduced rate improved protein delivery without caloric overfeeding.

Nutrition in the ICU: new trends versus old-fashioned standard enteral feeding?

The narrative review aims to summarize the relevant studies from the last 2 years and provide contextual information to understand findings. Recent ICU studies have provided insight in the pathophysiology and time course of catabolism, anabolic resistance, and metabolic and endocrine derangements interacting with the provision of calories and proteins.Early provision of high protein intake and caloric overfeeding may confer harm. Refeeding syndrome warrants caloric restriction and to identify patients at risk phosphate monitoring is mandatory.Infectious complications of parenteral nutrition are associated with overfeeding. In recent studies enteral nutrition is no longer superior over parenteral nutrition.Previously reported benefits of glutamine, selenium, and fish oil seem to have vanished in recent studies; however, studies on vitamin C, thiamine, and corticosteroid combinations show promising results. Studies from the last 2 years will have marked impact on future nutritional support strategies and practice guidelines for critical care nutrition as they challenge several old-fashioned concepts.

Investigation of adipocyte proteome during the differentiation of brown preadipocytes

Brown adipocytes oxidize fatty acids to produce heat in response to cold or caloric overfeeding. The motivation and function of the development of brown fat may thus counteract obesity, though this remains uncertain. We investigated the brown adipocyte proteome by two-dimensional gel electrophoresis followed by mass spectrometry. Comparative analyses of proteins focused on total protein spots to filter differentially expressed proteins during the differentiation of mouse primary brown preadipocytes. A Western blot analysis was performed to verify the target proteins. The results indicated that 10 protein spots were differentially expressed with significant changes, including the three up-regulated proteins of prohibitin, hypoxanthine-guanine phosphoribosyltransferase, and enoyl-CoA hydratase protein; the 5 down-regulated proteins of triosephosphate isomerase, elongation factor 2, α-tropomyosin slow, endophilin-B1, and cofilin-1 (CFL1); and the two unequivocally expressed proteins of peroxiredoxin-1 and collagen α-1(i) chain precursor. We found that during brown adipogenesis, CFL1 has an inhibitory effect on brown adipocyte differentiation. The overexpression of CFL1 inhibited the brown fat deposition and repressed the brown marker genes UCP1, PRDM16, PGC-1α and PPARγ via actin dynamics and polymerization. These observations may be novel findings that bring new insight into the detailed mechanisms of brown adipogenesis and identify possible therapeutic targets for anti-obesity. We use 2-DE to compare the proteomes of adipocytes during the brown adipogenesis of primary mouse preadipocytes. We identified 10 proteins that are differentially expressed. Among these, we found that the actin binding protein CFL1 inhibits the differentiation of brown preadipocytes. CFL1 overexpressing cells showed lower deposition of brown fat droplets, and the brown marker genes of UCP1, PRDM16, PGC-1α and PPARγ were decreased through actin dynamics and polymerization.

International residency for the development of the emergency department clinical nurse specialist role

Brown adipocytes oxidize fatty acids to produce heat in response to cold or caloric overfeeding. The motivation and function of the development of brown fat may thus counteract obesity, though this remains uncertain. We investigated the brown adipocyte proteome by two-dimensional gel electrophoresis followed by mass spectrometry. Comparative analyses of proteins focused on total protein spots to filter differentially expressed proteins during the differentiation of mouse primary brown preadipocytes. A Western blot analysis was performed to verify the target proteins. The results indicated that 10 protein spots were differentially expressed with significant changes, including the three up-regulated proteins of prohibitin, hypoxanthine–guanine phosphoribosyltransferase, and enoyl-CoA hydratase protein; the 5 down-regulated proteins of triosephosphate isomerase, elongation factor 2, α-tropomyosin slow, endophilin-B1, and cofilin-1 (CFL1); and the two unequivocally expressed proteins of peroxiredoxin-1 and collagen α-1(i) chain precursor. We found that during brown adipogenesis, CFL1 has an inhibitory effect on brown adipocyte differentiation. The overexpression of CFL1 inhibited the brown fat deposition and repressed the brown marker genes UCP1, PRDM16, PGC-1α and PPARγ via actin dynamics and polymerization. These observations may be novel findings that bring new insight into the detailed mechanisms of brown adipogenesis and identify possible therapeutic targets for anti-obesity.We use 2-DE to compare the proteomes of adipocytes during the brown adipogenesis of primary mouse preadipocytes. We identified 10 proteins that are differentially expressed. Among these, we found that the actin binding protein CFL1 inhibits the differentiation of brown preadipocytes. CFL1 overexpressing cells showed lower deposition of brown fat droplets, and the brown marker genes of UCP1, PRDM16, PGC-1α and PPARγ were decreased through actin dynamics and polymerization.

Defective regulation of adipose tissue autophagy in obesity

Autophagy is a highly regulated process that has an important role in the control of a wide range of cellular functions, such as organelle recycling, nutrient availability and tissue differentiation. A recent study has shown an increased autophagic activity in the adipose tissue of obese subjects, and a role for autophagy in obesity-associated insulin resistance was proposed. Body mass reduction is the most efficient approach to tackle insulin resistance in over-weight subjects; however, the impact of weight loss in adipose tissue autophagy is unknown. Adipose tissue autophagy was evaluated in mice and humans. First, a mouse model of diet-induced obesity and diabetes was maintained on a 15-day, 40% caloric restriction. At baseline, markers of autophagy were increased in obese mice as compared with lean controls. Upon caloric restriction, autophagy increased in the lean mice, whereas it decreased in the obese mice. The reintroduction of ad libitum feeding was sufficient to rapidly reduce autophagy in the lean mice and increase autophagy in the obese mice. In the second part of the study, autophagy was evaluated in the subcutaneous adipose tissue of nine obese-non-diabetic and six obese-diabetic subjects undergoing bariatric surgery for body mass reduction. Specimens were collected during the surgery and approximately 1 year later. Markers of systemic inflammation, such as tumor necrosis factor-1α, interleukin (IL)-6 and IL-1β were evaluated. As in the mouse model, human obesity was associated with increased autophagy, and body mass reduction led to an attenuation of autophagy in the adipose tissue. Obesity and caloric overfeeding are associated with the defective regulation of autophagy in the adipose tissue. The studies in obese-diabetic subjects undergoing improved metabolic control following calorie restriction suggest that autophagy and inflammation are regulated independently.

Difficulty in administration of liquid protein solution via an enteral feeding tube

Patients with head or other trauma, thermal injury, or obesity may require aggressive protein supplementation beyond the protein content of commercially-available enteral feeding solutions.1,–3 Use of protein supplementation as adjuvant therapy to a liquid enteral nutrition formula is particularly useful when trying to avoid caloric overfeeding of the critically ill patient while maintaining an aggressive protein intake. Our previous approach toward meeting these increased protein requirements has been to use a protein powder supplement that, unfortunately, has been discontinued by the manufacturer. As a result, we employed the use of a liquid protein supplement as adjuvant therapy to the polymeric enteral feeding formula. These liquid protein supplements are a concentrated protein solution (1 g/2 mL) and their administration is usually in bolus increments one to four times daily via an enteral feeding tube. We discovered that the liquid protein solution could not be administered via feeding tube without dilution because significant resistance occurred when attempting to administer the solution via a small-bore feeding tube. The amount of dilution necessary for an adequate reduction in resistance was not standardized, and the nursing staff were often diluting the protein solution with variable volumes of water with each administration period. As a result of this difficulty in medication administration, some nurses became frustrated and doses were sometimes omitted.

A.S.P.E.N. Clinical Guidelines: Nutrition Support of the Critically Ill Child

careful selection of the appropriate mode of feeding and monitoring the success of the feeding strategy. The use of specific nutrients, which possess a drug-like effect on the immune or inflammatory state during critical illness, continues to be an exciting area of investigation. The lack of systematic research and clinical trials on various aspects of nutrition support in the PICU is striking and makes it challenging to compile evidence based practice guidelines. There is an urgent need to conduct well-designed, multicenter trials in this area of clinical practice. The extrapolation of data from adult critical care literature is not desirable and many of the interventions proposed in adults will have to undergo systematic examination and careful study in critically ill children prior to their application in this population. In the following sections, we will discuss some of the key aspects of nutrition support therapy in the PICU; examine the literature and provide best practice guidelines based on evidence from PICU patients, where available. While some PICU popu lations include neonates, A.S.P.E.N. Clinical Guidelines for neonates will be published as a separate series.

Preoperative protein and energy intake and postoperative complications in well-nourished, non-hospitalized elderly cardiac surgery patients

Little is known about the impact of preoperative protein or energy intake in relation to the occurrence of postoperative complications in patients who are not undernourished but cannot keep up their daily protein or energy requirements prior to cardiac surgery. Therefore, a prospective study on intake in preoperatively well-nourished, non-hospitalized cardiac surgery patients (>or= 65 y) was carried out. Between December 2004 and November 2005 preoperative protein and energy intake and postoperative outcome data were collected from 100 consecutive patients undergoing cardiac surgery. Comparison of low protein intake (<or= 0.98 g/kg/d) with high protein intake (>0.98 g/kg/d) showed a low protein intake did not result in more complications or prolonged length of stay. In low-risk operation patients in particular, a high-energy intake (>22 kcal/kg/d) resulted in more postoperative complications than a low energy intake (<or= 22 kcal/kg/d) (33.3% and 13.2%, respectively; (OR 5.0 95% CI [1.5-16.9])). A preoperative protein intake <or= 0.80 g/kg/d was seen in 22.6%, and an energy intake <or= 25 kcal/kg/d in 72.2% of the patients. The outcome of this study suggests that detecting and correcting a preoperative low protein or energy intake is of no clinical relevance in the well-nourished, non-hospitalized elderly cardiac surgery patients. Caloric overfeeding may be associated with an increased complication rate.

C-Reactive protein-determined injury severity: Length of stay predictor in surgical infants

Background/Purpose Serum C-reactive protein (CRP) levels reflect the severity of the metabolic response to injury in critically ill children. During this period, caloric overfeeding can increase complications and delay recovery. The authors hypothesized that by avoiding excessive caloric delivery, the effect of injury severity would be the major factor determining clinical outcome. Methods Twenty-eight surgical infants who had indirect calorimetry measurements while in the Neonatal Intensive Care Unit between August 2000 and January 2002 were studied. Serum CRP concentrations, mean energy expenditure (MEE), respiratory quotient (RQ), length of hospital stay (LOS), and caloric intake (I) at the time of indirect calorimetry were recorded. Data were analyzed using the Pearson product-moment correlation. Results Peak serum CRP was significantly correlated to LOS in all patients (r = 0.79, P < .0001). When net caloric balance (I-MEE) did not exceed 5 kcal/kg/d (n = 9), peak serum CRP was correlated positively with RQ (r = 0.66, P = .05). When I-MEE exceeded 5 kcal/kg/d (n = 19), the positive correlation of serum CRP with RQ was diminished (r = 0.23, P = .33). Conclusions CRP-measured injury severity is a major determinant of clinical outcome in surgical infants. In addition, overfeeding causes additional RQ elevation.

Thyroid hormone metabolism in obesity.

Serum thyroid hormone concentrations and their metabolic fate are within the normal range limits in obese subjects. Also serum TSH concentrations and its response to TRH are normal, suggesting that tissue availability of thyroid hormones is normally preserved in these subjects. In contrast, during caloric restriction serum T3 concentrations decrease as a consequence of its reduced production rate from peripheral deiodination of T4. Opposite, serum rT3 concentrations markedly increase as a result of its decreased metabolic clearance rate. During caloric overfeeding serum T3 concentration increase whereas serum rT3 concentrations decrease. In this condition the production rate of T3 increases. During caloric restriction and overfeeding serum T4 concentrations and its production and degradation are not modified.