Saturated Fats: A Perspective from Lactation and Milk Composition

For recommendations of specific targets for the absolute amount of saturated fat intake, we need to know what dietary intake is most appropriate? Changing agricultural production and processing to lower the relative quantities of macronutrients requires years to accomplish. Changes can have unintended consequences on diets and the health of subsets of the population. Hence, what are the appropriate absolute amounts of saturated fat in our diets? Is the scientific evidence consistent with an optimal intake of zero? If not, is it also possible that a finite intake of saturated fats is beneficial to overall health, at least to a subset of the population? Conclusive evidence from prospective human trials is not available, hence other sources of information must be considered. One approach is to examine the evolution of lactation, and the composition of milks that developed through millennia of natural selective pressure and natural selection processes. Mammalian milks, including human milk, contain 50% of their total fatty acids as saturated fatty acids. The biochemical formation of a single double bond converting a saturated to a monounsaturated fatty acid is a pathway that exists in all eukaryotic organisms and is active within the mammary gland. In the face of selective pressure, mammary lipid synthesis in all mammals continues to release a significant content of saturated fatty acids into milk. Is it possible that evolution of the mammary gland reveals benefits to saturated fatty acids that current recommendations do not consider

A reappraisal of the impact of dairy foods and milk fat on cardiovascular disease risk

Background This review provides a reappraisal of the potential effects of dairy foods, including dairy fats, on cardiovascular disease (CVD)/coronary heart disease (CHD) risk. Commodities and foods containing saturated fats are of particular focus as current public dietary recommendations are directed toward reducing the intake of saturated fats as a means to improve the overall health of the population. A conference of scientists from different perspectives of dietary fat and health was convened in order to consider the scientific basis for these recommendations. Aims This review and summary of the conference focus on four key areas related to the biology of dairy foods and fats and their potential impact on human health: (a) the effect of dairy foods on CVD in prospective cohort studies; (b) the impact of dairy fat on plasma lipid risk factors for CVD; (c) the effects of dairy fat on non-lipid risk factors for CVD; and (d) the role of dairy products as essential contributors of micronutrients in reference food patterns for the elderly. Conclusions Despite the contribution of dairy products to the saturated fatty acid composition of the diet, and given the diversity of dairy foods of widely differing composition, there is no clear evidence that dairy food consumption is consistently associated with a higher risk of CVD. Thus, recommendations to reduce dairy food consumption irrespective of the nature of the dairy product should be made with cautionJ. Bruce German, Robert A. Gibson, Ronald M. Krauss, Paul Nestel, Benoît Lamarche, Wija A. van Staveren, Jan M. Steijns, Lisette C. P. G. M. de Groot, Adam L. Lock and Frédéric Destaillat

Effects of rhG-CSF on neutrophil functions and survival in sepsis induced diabetic rats

Diabetic patients are more prone to infection and evidence for an immunologic defect superimposed upon the metabolic abnormalities of diabetes is convincing. Neutrophils play a critical role in the host defense mechanism against various bacterial infections, and it is suggested that impaired neutrophil functions cause susceptibility to infections in diabetic patients. To explore the possibility that Granulocyte colony-stimulating factor (G-CSF) may be useful to prevent the morbidity and mortality caused by infections in diabetics. We studied the effect of G-CSF against septicemia in diabetic rats

Effects of granulocyte-macrophage colony-stimulating factor on incisional wound healing in an experimental diabetic rat model

The exact nature of poor wound healing in diabetes is uncertain. Neutrophils play a critical role in the host defense mechanism, and it is suggested that impaired neutrophil functions cause healing difficulties with or without infections in diabetic patients. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is used clinically when given systematically to increase the circulating neutrophils, but its wound-healing effects have not been systematically studied. This study was undertaken to examine the effects of GM-CSF on incisional wound healing in an experimental diabetic rat model. Forty rats were randomly divided into three groups, group I receiving saline as control, diabetes-induced group II receiving saline and diabetes-induced group III receiving GM-CSF. The anesthetized rats in all groups were wounded 21 days after diabetes induction by streptozotocin. Blood neutrophil counts and neutrophil fractions were also determined three days after wounding. Tensile strengths of wounded skin and the hydroxyproline (hyp) level of the wound were determined and wound healing processes were evaluated by light and electron microscopy, fourteen days after wounding. Neutrophil counts and phagocytosis were significantly increased in group III and neutrophil counts decreased in group II (p < 0.05). Although the hydroxyproline level of wound tissue significantly decreased in group II as compared with group III (p < 0.05), there was no differences of tensile strength between group II and III (p < 0.05). Wound score in group II was less than that in groups I and III (p < 0.05). It is concluded that PMN may have a role in modulating wound healing. GM-CSF may be useful for creating better wound healing healing. GM-CSF may be useful for creating better wound healing in risky patients such as diabetics

The relationship between neutrophils and incisional wound healing

The systemic administration of granulocyte-macrophage colony-stimulating factor (GMCSF) is used clinically to increase circulating neutrophils, but its wound healing effects after intraperitoneal treatment have not been studied yet. We planned to investigate the effect of neutrophils on wound healing under cyclophosphamide and GM-CSF treatment. Forty rats were divided into three groups: control group (group I, n = 12) receiving saline, group II (n = 14) receiving cyclophosphamide and group III (n = 14) receiving GM-CSF. The rats in all groups underwent incisional wounding and were euthanized after 7 days. Blood neutrophil counts and functions, tensile strengths and the hydroxyproline level of skin were determined, and a histopathological evaluation of healing was made. Neutrophil counts and phagocytosis significantly increased in group III and decreased in group II. Although the skin hydroxyproline level did not differ, there was a difference in tensile strength of the wounded skin between group II and group III. The wound score in group II was lower than that in groups III and I. As a result we suggest that systemically given GM-CSF - by increasing the neutrophil count and neutrophil phagocytosis index - can enhance the tensile strength of surgical incisions. Copyright (C) 2001 S. Karger AG, Basel

formation

Objective: To investigate the potential role of mast cell stabilisation in the prevention of post-operative adhesions.Design: Laboratory animal experiment.Setting: University hospital, Turkey,Subjects: Ninety Wistar albino rats.Intervention: Under anaesthesia, a lower midline laparotomy was performed, the caecum exposed and grasped until haemorrhage occurred. The rats were divided into three groups. Group 1, 2 and 3 were intra-peritoneally administered 1 mi of saline, disodium cromoglycate 5mg/kg in 1 ml of saline and 10mg/kg in 1 ml of saline, respectively thirty minutes prior to laparotomy and immediately subsequent to abdominal closure. They were later sacrificed, laparotomy repeated and the presence and extent of intra-abdominal adhesions evaluated.Results: Adhesion scores were best in the high disodium cromoglycate dose group of rats (p<0.05) and the number of degranulated mast cells was significantly low in this group (p<0.05),Conclusion: Disodium cromoglycate may be an effective agent for attenuating adhesion formation when administered in suitable doses

formation

Objective: To investigate the potential role of mast cell stabilisation in the prevention of post-operative adhesions.Design: Laboratory animal experiment.Setting: University hospital, Turkey,Subjects: Ninety Wistar albino rats.Intervention: Under anaesthesia, a lower midline laparotomy was performed, the caecum exposed and grasped until haemorrhage occurred. The rats were divided into three groups. Group 1, 2 and 3 were intra-peritoneally administered 1 mi of saline, disodium cromoglycate 5mg/kg in 1 ml of saline and 10mg/kg in 1 ml of saline, respectively thirty minutes prior to laparotomy and immediately subsequent to abdominal closure. They were later sacrificed, laparotomy repeated and the presence and extent of intra-abdominal adhesions evaluated.Results: Adhesion scores were best in the high disodium cromoglycate dose group of rats (p<0.05) and the number of degranulated mast cells was significantly low in this group (p<0.05),Conclusion: Disodium cromoglycate may be an effective agent for attenuating adhesion formation when administered in suitable doses

Novel insights into the function and dynamics of extracellular matrix in liver fibrosis

Emerging evidence suggests that altered components and posttranslational modifications of proteins in the extracellular matrix (ECM) may both initiate and drive disease progression. The ECM is a complex grid consisting of multiple proteins, most of which play a vital role in containing the essential information needed for maintenance of a sophisticated structure anchoring the cells and sustaining normal function of tissues. Therefore, the matrix itself may be considered as a paracrine/endocrine entity, with more complex functions than previously appreciated. The aims of this review are to 1) explore key structural and functional components of the ECM as exemplified by monogenetic disorders leading to severe pathologies, 2) discuss selected pathological posttranslational modifications of ECM proteins resulting in altered functional (signaling) properties from the original structural proteins, and 3) discuss how these findings support the novel concept that an increasing number of components of the ECM harbor signaling functions that can modulate fibrotic liver disease. The ECM entails functions in addition to anchoring cells and modulating their migratory behavior. Key ECM components and their posttranslational modifications often harbor multiple domains with different signaling potential, in particular when modified during inflammation or wound healing. This signaling by the ECM should be considered a paracrine/endocrine function, as it affects cell phenotype, function, fate, and finally tissue homeostasis. These properties should be exploited to establish novel biochemical markers and antifibrotic treatment strategies for liver fibrosis as well as other fibrotic diseases