Satiety Innovations: Food Products to Assist Consumers with Weight Loss, Evidence on the Role of Satiety in Healthy Eating: Overview and In Vitro Approximation

2016 ◽  
Vol 5 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Rubén López-Nicolás ◽  
Massimo Marzorati ◽  
Lia Scarabottolo ◽  
Jason C. G. Halford ◽  
Alexandra M. Johnstone ◽  
...  
Author(s):  
Mari Niva

This study examines the slimming practice produced by Internet-based weight-loss services and their use. Drawing on theories of practice, the study analyses the script of use that is constructed by the services, and the meanings, materialities and competences that are enacted in their use. Based on 20 semi-structured interviews with women who were users of two Finnish online weight-loss services, the study concludes that the services transform food into quantitative depictions of calories and nutrition. They configure slimmers as calculative agents and slimming as a practice based on incessant recording and monitoring. For online slimmers, the services acted in the double role of a control device with a focus on calorie restriction, and a learning device used to develop a skill of healthy eating. In the latter role, online slimming was hoped to result in an internalisation of a lifestyle change that would make calculation and constant monitoring unnecessary and the services redundant for their users. The results suggest that for its practitioners, online slimming is temporary rather than long-standing, but it may and is expected to act as a mediary in establishing other practices related to healthy lifestyles.


Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2363-2373 ◽  
Author(s):  
WR Drobyski ◽  
CA Keever ◽  
GA Hanson ◽  
T McAuliffe ◽  
OW Griffith

The pathophysiologic role of nitric oxide (NO) in graft-versus-host disease (GVHD) was investigated in a murine bone marrow (BM) transplantation model where donor and recipient were H-2-matched but differed at multiple minor histocompatibility antigens. Host AKR/J (H- 2K) mice received lethal total body irradiation as pretransplant conditioning followed by transplantation of donor B10.BR (H-2K) BM cells with or without spleen cells as a source of GVH-reactive T cells. NO production, as assessed by serum nitrate and nitrite levels, was increased for up to 3 weeks posttransplant in animals undergoing both moderate and severe GVHD. Administration of NG-methyl-L-arginine (L- NMA), an inhibitor of nitric oxide synthase, to animals undergoing GVHD resulted in effective suppression of NO production when compared with saline-treated GVHD control animals. Suppression of NO production by L- NMA in GVHD animals was associated with enhanced weight loss early posttransplant and decreased overall survival. Histologic analysis of tissues from L-NMA-treated and saline-treated GVHD animals showed that early weight loss was not because of an exacerbation of GVHD, indicating that NO did not appear to play an immunosuppressive role in this experimental model. L-NMA-treated animals with enhanced weight loss were observed to have splenic atrophy, decreased extramedullary hematopoiesis, and a reduction in BM cellularity when compared with GVHD control mice that were weight-matched before transplant. Analysis of T-cell chimerism in the spleen showed that L-NMA treatment impaired donor T-cell repopulation. In vitro colony-forming unit (CFU) assays were performed to further assess the role of NO on BM progenitor cell growth. L-NMA added directly into culture had no effect on CFU- granulocyte/macrophage (CFU-GM) formation in normal murine BM. In contrast, total CFU-GM from L-NMA-treated animals were significantly reduced when compared with GVHD controls or BM control animals who did not develop GVHD. Collectively, these data indicate that inhibition of NO impairs hematopoietic reconstitution and support the premise that NO appears to play a novel role in the facilitation of alloengraftment posttransplant.


2020 ◽  
Author(s):  
Yuejin Liang ◽  
Panpan Yi ◽  
Wenjuan Ru ◽  
Zuliang Jie ◽  
Hui Wang ◽  
...  

Abstract Background The Zika virus (ZIKV) outbreak that occurred in multiple countries was linked to increased risk of neurological disorders and congenital defects. However, host immunity and immune-mediated pathogenesis in ZIKV infection are not well understood. Interleukin-22 (IL-22) is a crucial cytokine for regulating host immunity in infectious diseases. Whether IL-22 plays a role in ZIKV infection is unknown. Methods The cellular source of IL-22 was identified in IFNAR−/− mice and WT neonatal mice during ZIKV infection. To determine the role of IL-22, we challenged 1-day-old wild-type (WT) and IL-22−/− mice with ZIKV and monitored clinical manifestations. Glial cell activation in the brain was assessed by confocal imaging. ZIKV-specific CD8+ T cell responses in both the spleen and brain were analyzed by flow cytometry. In addition, we infected mouse primary astrocytes in vitro, and characterized the reactive astrocyte phenotype. Human glial cell line was also infected with ZIKV in the presence of IL-22, followed by the evaluation of cell proliferation, cytokine expression and viral loads. Results We found that γδ T cells were the main source of IL-22 during ZIKV infection in both the spleen and brain. WT mice began to develop weight loss, staggered steps, bilateral hind limb paralysis, weakness at 10 days post-infection (dpi), and ultimately succumbed to infection at 16–19 dpi. Surprisingly, IL-22 deficiency lessened weight loss, moderated the systemic inflammatory response, and greatly reduced the incidence of neurological disorders and mortality. ZIKV infection facilitated a neurotoxic polarization of A1-prone astrocytes in vitro. Additional analysis demonstrated that the absence of IL-22 resulted in reduced activation of microglia and astrocytes in the cortex. Although IL-22 displayed a marginal effect on glial cells in vitro, IL-22−/− mice mounted more vigorous ZIKV-specific CD8+ T cell responses, which led to a more effective control of ZIKV in the brain. Conclusions Our data revealed a pathogenic role of IL-22 in ZIKV encephalitis.


Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2363-2373 ◽  
Author(s):  
WR Drobyski ◽  
CA Keever ◽  
GA Hanson ◽  
T McAuliffe ◽  
OW Griffith

Abstract The pathophysiologic role of nitric oxide (NO) in graft-versus-host disease (GVHD) was investigated in a murine bone marrow (BM) transplantation model where donor and recipient were H-2-matched but differed at multiple minor histocompatibility antigens. Host AKR/J (H- 2K) mice received lethal total body irradiation as pretransplant conditioning followed by transplantation of donor B10.BR (H-2K) BM cells with or without spleen cells as a source of GVH-reactive T cells. NO production, as assessed by serum nitrate and nitrite levels, was increased for up to 3 weeks posttransplant in animals undergoing both moderate and severe GVHD. Administration of NG-methyl-L-arginine (L- NMA), an inhibitor of nitric oxide synthase, to animals undergoing GVHD resulted in effective suppression of NO production when compared with saline-treated GVHD control animals. Suppression of NO production by L- NMA in GVHD animals was associated with enhanced weight loss early posttransplant and decreased overall survival. Histologic analysis of tissues from L-NMA-treated and saline-treated GVHD animals showed that early weight loss was not because of an exacerbation of GVHD, indicating that NO did not appear to play an immunosuppressive role in this experimental model. L-NMA-treated animals with enhanced weight loss were observed to have splenic atrophy, decreased extramedullary hematopoiesis, and a reduction in BM cellularity when compared with GVHD control mice that were weight-matched before transplant. Analysis of T-cell chimerism in the spleen showed that L-NMA treatment impaired donor T-cell repopulation. In vitro colony-forming unit (CFU) assays were performed to further assess the role of NO on BM progenitor cell growth. L-NMA added directly into culture had no effect on CFU- granulocyte/macrophage (CFU-GM) formation in normal murine BM. In contrast, total CFU-GM from L-NMA-treated animals were significantly reduced when compared with GVHD controls or BM control animals who did not develop GVHD. Collectively, these data indicate that inhibition of NO impairs hematopoietic reconstitution and support the premise that NO appears to play a novel role in the facilitation of alloengraftment posttransplant.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e15711-e15711
Author(s):  
Howard Bruckner ◽  
Azriel Hirschfeld ◽  
Daniel Gurell ◽  
King Lee

e15711 Background: High dose ascorbic acid inhibits many tumors in vitro. It may reduce chemotherapy's adverse hematologic events and improve quality of life. Moderate dose gemcitabine, fluorouracil, leucovorin, irinotecan, oxaliplatin (GFLIP) is an effective regimen for patients with many cancers (Anticancer Research 17). High dose ascorbic acid may reverse half the preexisting and largely eliminate the predicted cumulative toxicity of GFLIP (ASCO 15). Methods: High dose ascorbic acid AA 75-100 grams IV was given 1-2 times per week with GFLIP every 2 weeks until progression with serial wkly and Q2wk blood tests and 3 month imaging. Eligibility: Unresectable, III, recurrent and metastatic, mod and high grade typical pancreatic ca; ECOG 0-2; +/- prior chemo; adults of any age with consent. Results: A prescheduled 2 yr analysis found 26 patients; 16 ≥ 65, (9 ≥ 70 years of age). 25 stage IV; Nine had failed at least one prior standard chemo (35%), 3 were PS 2, 9 had severe weight loss. Safety: Five had uncomplicated 3 (19%) and none had 4 neutropenia or neutropenic infection, one (4%) had a 3 anemia and thrombocytopenia without bleeding. Prophylactic growth factors were not used and limited to 1-2 as needed low doses used infrequently. There was no limiting diarrhea, enteritis, stomatitis, weight loss or coagulopathy due to GFLIP. GFLIP is on track to reproduce/retain prior response and survival benefit (ASCO 08). Conclusions: Ascorbic Acid-GFLIP can be exceptionally safe and well tolerated. It may avoid standard 20-40% rates of severe toxicities. It can be, otherwise unavailable, safe reduced cost, treatment for many elderly and prior resistant tumor patients. Given the broad multi-disease role of the GFLIP drugs, and available personalized medicine tests (Cancer Letters), further development is very attractive and feasible. Potential outcome can spare all, and especially high risk pancreatic ca patients, 20k severe toxicities every year toxicities as much as $100 million cost and make some ineligibility criteria unnecessary. Development of safe AA regimens may benefit quality of life and improve survival for many with a broad spectrum of cancers that otherwise go untreated. Clinical trial information: NCT01905150.


1983 ◽  
Vol 245 (3) ◽  
pp. R396-R402
Author(s):  
R. B. Melnyk ◽  
N. Mrosovsky ◽  
J. M. Martin

Dormice (Glis glis) undergo spontaneous cyclic changes in food intake and body weight. These infradian cycles with a periodicity of about 2 mo are endogenously controlled, since they persist in conditions of constant temperature and photoperiod. To evaluate the role of insulin as an effector of hyperphagia and fattening in dormice, experiments were conducted to study pancreatic function and adipose tissue metabolism during several phases of the infradian cycle. During the weight loss phase, peripheral insulin resistance occurs in the absence of hyperinsulinism. This resistance is not corrected by weight loss. Weight loss phase animals showed poor glucose tolerance and an impaired in vitro glucose-stimulated insulin secretion; these were not attributable to reduced pancreatic insulin content. Although basal glucose transport and basal, as well as insulin-stimulated, glucose utilization in isolated adipocytes were depressed during the weight loss phase, insulin-stimulated transport was significant. The data offer no evidence that insulin has a direct causal role in the development of spontaneous obesity in this species.


Author(s):  
Janet H. Woodward ◽  
D. E. Akin

Silicon (Si) is distributed throughout plant tissues, but its role in forages has not been clarified. Although Si has been suggested as an antiquality factor which limits the digestibility of structural carbohydrates, other research indicates that its presence in plants does not affect digestibility. We employed x-ray microanalysis to evaluate Si as an antiquality factor at specific sites of two cultivars of bermuda grass (Cynodon dactvlon (L.) Pers.). “Coastal” and “Tifton-78” were chosen for this study because previous work in our lab has shown that, although these two grasses are similar ultrastructurally, they differ in in vitro dry matter digestibility and in percent composition of Si.Two millimeter leaf sections of Tifton-7 8 (Tift-7 8) and Coastal (CBG) were incubated for 72 hr in 2.5% (w/v) cellulase in 0.05 M sodium acetate buffer, pH 5.0. For controls, sections were incubated in the sodium acetate buffer or were not treated.


Author(s):  
David B. Warheit ◽  
Lena Achinko ◽  
Mark A. Hartsky

There is a great need for the development of a rapid and reliable bioassay to evaluate the pulmonary toxicity of inhaled particles. A number of methods have been proposed, including lung clearance studies, bronchoalveolar lavage analysis, and in vitro cytotoxicity tests. These methods are often limited in scope inasmuch as they measure only one dimension of the pulmonary response to inhaled, instilled or incubated dusts. Accordingly, a comprehensive approach to lung toxicity studies has been developed.To validate the method, rats were exposed for 6 hours or 3 days to various concentrations of either aerosolized alpha quartz silica (Si) or carbonyl iron (CI) particles. Cells and fluids from groups of sham and dust-exposed animals were recovered by bronchoalveolar lavage (BAL). Alkaline phosphatase, LDH and protein values were measured in BAL fluids at several time points postexposure. Cells were counted and evaluated for viability, as well as differential and cytochemical analysis. In addition, pulmonary macrophages (PM) were cultured and studied for morphology, chemotaxis, and phagocytosis by scanning electron microscopy.


2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.


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