To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Small for gestational age (SGA) is typically defined as birth weight < 10th percentile for age. Limited data are available regarding the growth of SGA preterm infants in relation to feeding type. We aimed to study SGA preterm infants fed fortified mother’s own milk (MOM) or preterm formula (PF) on growth patterns and catch-up growth at discharge and 2-year corrected age (CA). Our retrospective cohort study included data from medical records and follow-up questionnaires about SGA preterm infants born at < 37 weeks fed on MOM (n 40) and PF (n 40). Weight, length/height and head circumference (HC) were collected at birth, discharge and at 2-year CA, and Δ z-scores were calculated. The MOM group had significantly larger negative change in weight and length z-scores between birth and discharge, and smaller positive change in HC z-score (–0·47 (sd 0·41) v. −0·25 (sd 0·36), P = 0·01; −0·63 (sd 0·75) v. −0·27 (sd 0·75), P = 0·03; 0·13 (sd 0·67) v. 0·41 (sd 0·55), P = 0·04, respectively). Almost half of the MOM-fed infants experienced poor length growth by discharge compared with 22 % of PF-fed infants (P = 0·03). By 2-year CA, both groups had similar positive change in weight and HC z-scores, but MOM-fed infants had a slower increase in height z-score (0·64 (sd 1·30) v. 1·33 (sd 1·33), P = 0·02), and only 40 % had achieved catch-up height compared with 68 % of the PF group (P = 0·02). Our study indicates that fortified MOM-fed SGA preterm infants may need extra nutritional support in the first 2 years of life to achieve height growth potential.
To investigate the extent, quality and challenges of dietetic counselling during the pandemic.
A cross-sectional online thirty-six-item Google Survey. The survey queried demographics and information on usage and perceived telemedicine quality.
The survey was distributed to Israeli Dietetic Association (ATID) mailing list between 31 March and 5 May 2020.
Clinical dietitians, members of ATID, who consented to participated in the survey.
Three hundred dietitians (12 % of ATID members; 95 % women; mean age 4·41 (sd 10·2) years) replied to the survey. Most dietitians reported a significant ∼30 % decrease in work hours due to the pandemic. The most prevalent form of alternative nutrition counselling (ANC) was over the phone (72 %); 53·5 % used online platforms. Nearly 45 % had no former ANC experience. Both ANC formats were reported inferior to face-to-face nutritional consultation (consultation quality median scores 8 and 7, on a 1–10 scale, for online and phone, respectively). ANC difficulties on either phone or online platforms were technical (56 and 47 %, respectively), lack of anthropometric measurements (28 and 25 %, respectively) and interpersonal communication (19 and 14·6 %, respectively). Older age and former phone counselling experience were associated with higher quality scores, respectively (OR = 1·046, 95 % CI 1·01, 1·08, P = 0·005), (95 % CI 1·38, 4·52, P = 0·02). Those who continued to work full time had five-time greater odds for a higher quality score using online platforms (OR = 5·33, 95 % CI 1·091, 14·89, P = 0·001).
Our findings suggest telemedicine holds considerable promise for dietary consultation; however, additional tools and training are needed to optimise remote ANC, especially in light of potential crisis-induced lockdown.
Sustaining adequate nutritional needs of a population is a challenging task in normal times and a priority in times of crisis. There is no ‘one-size-fits-all’ solution that addresses nutrition. In relevance to the COVID-19 (coronavirus disease 2019) pandemic crisis, viral infections in general and RNA viruses in particular are known to induce and promote oxidative stress, consequently increasing the body’s demand for micronutrients, especially those related to antioxidant enzymic systems, thus draining the body of micronutrients, and so hindering the human body’s ability to cope optimally with oxidative stress. Common polymorphisms in major antioxidant enzymes, with world population minor allele frequencies ranging from 0·5 to 50 %, are related to altered enzymic function, with substantial potential effects on the body’s ability to cope with viral infection-induced oxidative stress. In this review we highlight common SNP of the major antioxidant enzymes relevant to nutritional components in the context of viral infections, namely: superoxide dismutases, glutathione peroxidases and catalase. We delineate functional polymorphisms in several human antioxidant enzymes that require, especially during a viral crisis, adequate and potentially additional nutritional support to cope with the pathological consequences of disease. Thus, in face of the COVID-19 pandemic, nutrition should be tightly monitored and possibly supplemented, with special attention to those carrying common polymorphisms in antioxidant enzymes.
Exocrine pancreatic digestive enzymes are essential for the digestion of dietary components and are regulated by them. Chronic excess dietary high fat (HF) consumption is a contributing factor of diet-induced obesity (DIO) and associated chronic diseases and requires adaptation by the pancreas. The aim of the present study was to investigate the effects of chronic HF diet feeding on exocrine pancreatic digestive enzyme transcript levels in DIO C57BL/6J mice. C57BL/6J mice were fed diets containing either 10 or 45 % energy (E%) derived from fat for 12 weeks (n 10 mice per diet group). Pancreatic tissue and blood samples were collected at 0, 4 and 12 weeks. The expression of a panel of exocrine pancreatic digestive enzymes was analysed using quantitative RT-PCR and Western blot analysis. The HF (45 E%) diet-fed C57BL/6J mice developed obesity, hyperleptinaemia, hyperglycaemia and hyperinsulinaemia. The transcript levels of pancreatic lipase (PL), pancreatic lipase-related protein 2 (PLRP2) and pancreatic phospholipase A2 (PLA2) were initially elevated; however, they were down-regulated to basal control levels at week 12. The transcript levels of colipase were significantly affected by diet and time. The protein levels of PL and PLRP2 responded to HF diet feeding. The transcript levels of amylase and proteases were not significantly affected by diet and time. The transcript levels of specific lipases in hyperinsulinaemic, hyperleptinaemic and hyperglycaemic DIO C57BL/6J mice are down-regulated. However, these mice compensate for this by the post-transcriptional regulation of the levels of proteins that respond to dietary fat. This suggests a complex regulatory mechanism involved in the modulation of fat digestion.
Leptin, a metabolic regulator of energy expenditure, exerts its peripheral effects primarily by altering lipid metabolism. The exocrine pancreas has a key role in the digestion of dietary lipids, but the role of leptin in regulating pancreatic lipases remains unknown. Using the exocrine pancreas in vitro AR42J cell model, we studied the direct effects of leptin on pancreatic lipase (PL) secretion and on the mRNA levels of PL and PL-related proteins 1 and 2 (PLRP1, PLRP2). Leptin directly, rapidly (within 30 min) and significantly inhibited both the secretion and intracellular activity of PL. Leptin downregulated mRNA levels of PL and PLRP1, and upregulated transcripts of PLRP2. This study provides the first evidence that leptin directly regulates exocrine lipases at the levels of synthesis, activity and secretion. This rapid regulation may be associated with a short-term control of energy balance.
Lactation alters maternal metabolism and increases food intake in rats to support milk production. Pancreatic lipase (PL) is primarily responsible for fat digestion in adults and is regulated by dietary fat. The present research determined the regulation of PL by lactation and dietary fat. In Expt 1, eighteen Sprague–Dawley dams and twelve age-matched virgins (controls) were fed a low-fat diet (LF; 11 % energy as safflower oil) for 7–63 d. At postpartum (day 0), peak lactation (day 15) and post-lactation (day 56) and after 7 d in virgins, the pancreas was removed for mRNA and enzyme analyses. In Expt 2, thirty-six Sprague–Dawley dams were fed LF until day 9 postpartum when dams were divided into three groups of twelve; one continued to be fed LF, one was fed a moderate-fat diet (MF; 40 % energy as safflower oil); and one was fed a high-fat diet (HF; 67 % energy as safflower oil) diet. At peak lactation (day 15) and post-lactation (day 56), the pancreas was removed for mRNA and enzyme analyses. Expt 1 revealed that lactation and post-lactation significantly (P<0·001) decreased PL mRNA (67 % and 76 %, respectively), but only post-lactation decreased PL activity. Increased dietary fat in Expt 2 significantly increased PL mRNA (LF<MF<HF, P<0·001) and PL activity (LF<MF=HF, P<0·02) in both lactation and post-lactation. In summary, lactation and post-lactation decreased PL mRNA significantly even though dietary fat still regulated PL activity and mRNA in lactation and post-lactation.
Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.
Email your librarian or administrator to recommend adding this to your organisation's collection.