Role of parenteral nutrition in bone, lean and fat mass variations during intestinal malabsorption syndrome

Introduction: Sedentary lifestyle and excessive calorie intake are risk factors for CVD. We have demonstrated the cardioprotective effect of exercise in aged mice and the critical role of visceral adiposity and its profibrotic secretome in increasing cardiovascular risks in obesity and aging. The association between exercise, lowered plasma leptin and reduced inflammatory leukocytes has been recently shown in patients with atherosclerosis. It remains unclear whether elevated plasma leptin can preserve or alter cardiovascular function in obesity. Methods: We analyzed the effect of high fat diet (HFD) in C57BL/6J male mice on the heart in terms of function, structure, histology and key molecular markers. Two interventions were used: 1) active fat mass loss via exercise (daily swimming) during HFD; 2) passive fat mass loss via surgical removal of the visceral adipose tissue (VAT lipectomy) followed by HFD. Results: HFD increased body weight and adiposity, leading to higher plasma leptin, glucose and insulin levels, compared to control diet (CD) mice. HFD impaired left ventricle (LV) structure (hypertrophy, interstitial fibrosis) and cardiac function (echocardiography, in vivo hemodynamics). Atria of HFD mice had enhanced pro-inflammatory protein production. Exercise reduced circulating leptin levels in HFD mice by 50%, in line with fat mass loss. In contrast, lipectomy reduced visceral fat mass, but body weight, adiposity and plasma leptin did not change. Both exercise and VAT lipectomy improved cardiac contractility, reversed collagen deposition and oxidative stress in HFD mice. Both interventions downregulated LV pro-inflammatory markers. We proved the role of leptin in cardiac remodeling in vitro by incubating primary cardiac fibroblasts with hyperleptinemic plasma from HFD mice. Remarkably, plasma from HFD-EX (exercise) suppressed the fibro-proliferative and pro-inflammatory responses of cardiac fibroblasts. Conclusions: Leptin directly contribute to cardiac fibrosis in obesity via activation and proliferation of cardiac fibroblasts. Understanding how leptin signals to the heart might have implications in a wide range of CVD, potentially helping early stratification and personalized care.

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Role of the Nurse in Peripheral Vein Needle Replacement

PEDIATRICS ◽

10.1542/peds.60.5.781 ◽

1977 ◽

Vol 60 (5) ◽

pp. 781-781

Author(s):

S. Gorham Babson ◽

Gerda I. Benda ◽

Jayant P. Shenai

Keyword(s):

Critical Care ◽

Parenteral Nutrition ◽

Total Parenteral Nutrition ◽

Health Sciences ◽

Peripheral Vein ◽

Neonatal Nurses ◽

Intravenous Infusions ◽

Oregon Health ◽

The University

We agree with Taeusch and Heafitz in their letter to the editor (Pediatrics 57:977, June 1976) that total or near total parenteral nutrition can be given through needles placed in peripheral veins for weeks and even months. Whether one uses the "Usher" needles or the "butterfly" model, the success in maintaining infusions depends on the ability and availability of the operator. In the NICC at the University of Oregon Health Sciences Center, neonatal nurses have had the responsibility of maintaining peripheral intravenous infusions in both medical and surgical infants for nearly ten years, involving several thousand neonates referred for critical care.

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Dissecting the Role of the Gut Microbiota and Diet on Visceral Fat Mass Accumulation (OR31-07-19)

Current Developments in Nutrition ◽

10.1093/cdn/nzz037.or31-07-19 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Author(s):

Caroline Le Roy ◽

Ruth Bowyer ◽

Claire Steves ◽

Tim Spector ◽

Bell Jordana

Keyword(s):

Vitamin E ◽

Random Forest ◽

Gut Microbiota ◽

Fat Mass ◽

Mediation Analysis ◽

Visceral Fat ◽

Nutrient Intake ◽

Microbiota Composition ◽

Gut Microbiota Composition

Abstract Objectives Accumulation of visceral fat mass (VFM) is a major risk factor for cardiovascular and metabolic disease. Both gut microbiota and diet have been shown to impact host adiposity in an interdependent manner, but the exact nature of their joint contributions has not been characterised. Here, we aimed to estimate and separate the effect of gut microbiota composition from that of nutrient intake on host VFM in of 1760 older female twins. Methods The gut microbiome profile was assessed by 16S sequencing. VFM was measured by DEXA whole body scan and nutrient intake was assessed through food frequency questionnaires. We used a combination of pair-wise associations, random forest modelling and mediation analysis to separate the effect of the gut microbiota and nutrients on VFM. Results Pairwise analyses revealed that 93 OTUs and 10 nutrients were significantly linked to VFM. Five of the 10 nutrients (fibre, trans fatty acids, magnesium, vitamin E and biotin) were also associated with 23% of the 93 VFM-associated OTUs. To separate the effects of the gut microbiota from nutrients on VFM we carried out conditional analyses. We observed that the majority (87%) of the 93 OTUs remained significantly associated with VFM irrespective of nutrient intake correction. In contrast, we observed that fibre, magnesium, biotin and vitamin E were no longer significantly associated with VFM when adjusting models for OTUs (P > 0.05), implying a role of the gut microbiota in mediating these nutrient effects on VFM. Formal mediation analysis revealed that the individual effect of fibre, biotin, magnesium and vitamin E on VFM were mediated at 69, 43, 41 and 31% respectively by OTUs. Moreover, we estimated that accumulated effect of OTUs on VFM (R2 = 0.19) was twice the one of nutrients (R2 = 0.11) and so were their prediction potential determined using random forest classification. Conclusions Our results suggest that while the role of certain nutrients on VFM appears to depend on gut microbiota composition, specific gut microbes may affect host adiposity regardless of dietary intake. The findings imply that the gut microbiota may have a greater contribution towards shaping host adiposity and VFM, compared to diet alone. Funding Sources We gratefully acknowledge support provided by the JPI HDHL funded DINAMIC consortium (administered by the MRC UK, MR/N030125/1). Supporting Tables, Images and/or Graphs

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The role of Chinese clinical pharmacists in parenteral nutrition for children using the Screening Tool Risk on Nutrititional Status and Growth (STRONGkids)

International Journal of Clinical Pharmacy ◽

10.1007/s11096-020-01156-4 ◽

2020 ◽

Author(s):

Ming-Mei Zhu ◽

Feng Chen ◽

Jing Xu ◽

Li-Hua Yuan ◽

Yong Zhang ◽

...

Keyword(s):

Parenteral Nutrition ◽

Screening Tool ◽

Clinical Pharmacists

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Nicotinamide Nucleotide Transhydrogenase (Nnt) is Related to Obesity in Mice

Hormone and Metabolic Research ◽

10.1055/a-1199-2257 ◽

2020 ◽

Vol 52 (12) ◽

pp. 877-881

Author(s):

Anne Kunath ◽

John T. Heiker ◽

Matthias Kern ◽

Joanna Kosacka ◽

Gesine Flehmig ◽

...

Keyword(s):

Fat Mass ◽

Metabolic Diseases ◽

Body Weight Gain ◽

Wild Type ◽

Inner Mitochondrial Membrane ◽

Nicotinamide Nucleotide Transhydrogenase ◽

Diet Induced Obesity ◽

Highly Sensitive ◽

Obesity In Mice

AbstractThe C57BL/6J (B6J) mouse strain has been widely used as a control strain for the study of metabolic diseases and diet induced obesity (DIO). B6J mice carry a spontaneous deletion mutation in the nicotinamide nucleotide transhydrogenase (Nnt) gene eliminating exons 7–11, resulting in expression of a truncated form of Nnt, an enzyme that pumps protons across the inner mitochondrial membrane. It has been proposed that this mutation in B6J mice is associated with epigonadal fat mass and altered sensitivity to diet induced obesity. To define the role of Nnt in the development of diet induced obesity, we generated first backcross (BC1) hybrids of wild type Nnt C57BL/6NTac and mutated Nnt C57BL/6JRj [(C57BL/6NTac×C57BL/6JRj)F1×C57BL/6NTac]. Body weight gain and specific fat-pad depot mass were measured in BC1 hybrids under high fat diet conditions. Both sexes of BC1 hybrids indicate that mice with Nnt wild type allele are highly sensitive to DIO and exhibit higher relative fat mass. In summary, our data indicate that the Nnt mutation in mice is associated with sensitivity to DIO and fat mass.

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