Implications of dietary α-linolenic acid in bone health

Recent evidence implies the benefit of ω-3 polyunsaturated fatty acids in bone health. Although eicosapentaenoic acid and docosahexaenoic acid, present in fish oil, have been extensively researched, much less is known about the influence of α-linolenic acid (ALA; present in flaxseeds), a metabolic precursor of eicosapentaenoic acid and docosahexaenoic acid, on bone. Our objective was to evaluate the published literature and distinguish between the individual effects of flaxseed oil and flax lignans on bone to elucidate the exact role of ALA in skeletal biology. The search was conducted in several databases resulting in 129 articles of which 30 were eligible for inclusion in this review. The studies showed that consumption of whole flaxseeds did not lead to a marked improvement of osteoporotic bones in humans and animals. However, when combined with estrogen therapy, flaxseed supplementation offered an extra benefit to bone in animal models. Similar results were found in studies conducted with flaxseed oil (predominantly ALA), but the favorable role of flaxseed oil was more obvious in various pathologic conditions (kidney disease, obesity with insulin resistance), resulting in improved bone properties. In contrast, despite a marginal estrogenic effect, the consumption of flax lignans resulted in little benefit to bone and the effect was limited to early life of females only in animal models. Based on the available studies, it could be concluded that supplementation with flaxseeds may contribute to some improvement in osteoporotic bone properties but the bone-protective effect may be attributed to ALA, not to the lignan fraction of flaxseeds.     

Discovery of MK-5046, a Potent,Selective Bombesin Receptor Subtype-3 Agonist for the Treatment of Obesity

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Tyrosinemia type II (Richner-Hanhart syndrome): a new mutation in the TAT gene

In the present study we report the clinical features and the molecular genetic investigation of the tyrosine aminotransferase (TAT) gene in a young girl from Croatia with Richner-Hanhart syndrome, mainly suffering from photophobia, hyperkeratosis of the palmes and soles and slight neurological abnormalities. Sequencing analysis of the TAT gene revealed a novel homozygous missense mutation c.1250G>A (p.R417Q) in exon 12, and herewith confirmed the clinical diagnosis. Showing the first symptoms in babyhood, at the age of 8 years it was for the first time clinically diagnosed that the patient suffers from tyrosinemia type II and a therapy with tyrosine and phenylalanine reduced diet has been started successfully. All symptoms disappeared within 2-4 weeks. Since that time, we have been following the girl until today for more than ten years. She is in a good condition, and attends the normal high school program.     

Gender-specific functional cerebral asymmetries and unilateral cerebral lesion sequelae

The magnitude and direction of cerebral lateralization are thought to be sexually dimorphic. Numerous human studies indicate gender-specific differences in functional cerebral asymmetries (FCAs) for various functions. Females are thought to have a decreased magnitude of inter-hemispheric cortical lateralization compared with males, whereas males exhibit a greater degree of cortical asymmetry than females for components of cognitive and perceptual processing. Also, a large body of evidence has shown that FCAs fluctuate across the menstrual cycle, presumably as a result of cycle-related hormonal changes. Awareness of gender-based differences of the human brain may enable better understanding of differences in functional outcome between men and women after unilateral cerebral lesion.     

Long-chain polyunsaturated fatty acids may mutually benefit both obesity and osteoporosis

The overconsumption of n-6 polyunsaturated fatty acids (PUFA), resulting in a high ratio of n-6 to n-3 PUFA, may contribute to the increased pathogenesis of obesity and osteoporosis by promoting low-grade chronic inflammation (LGCI). As evidence suggests, both obesity and osteoporosis are linked on a cellular and systemic basis. This review will analyze if a relationship exists between LGCI, fat, bone, and n-3 PUFA. During the life cycle, inflammation increases, fat mass accumulates, and bone mass declines, thus suggesting that a connection exists. This review will begin by examining how the current American diet and dietary guidelines may fall short of providing an anti-inflammatory dose of the n-3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). It will then define LGCI and outline the evidence for a relationship between fat and bone. Inflammation as it pertains to obesity and osteoporosis and how EPA and DHA can alleviate the associated inflammation will be discussed, followed by some preliminary evidence to show how mesenchymal stem cell (MSC) lineage commitment may be altered by inflammation to favor adipogenesis. Our hypothesis is that n-3 PUFA positively influence obesity and osteoporosis by reducing LGCI, ultimately leading to a beneficial shift in MSC lineage commitment. This hypothesis essentially relates the need for more focused research in several areas such as determining age and lifestyle factors that promote the shift in MSC commitment and if current intakes of EPA and DHA are optimal for fat and bone.     

Genotoxicity of metal nanoparticles: focus on in vivo studies

With increasing production and application of a variety of nanomaterials (NMs), research on their cytotoxic and genotoxic potential grows, as the exposure to these nano-sized materials may potentially result in adverse health effects. In large part, indications for potential DNA damaging effects of nanoparticles (NPs) originate from inconsistent in vitro studies. To clarify these effects, the implementation of in vivo studies has been emphasised. This paper summarises study results of genotoxic effects of NPs, which are available in the recent literature. They provide indications that some NP types cause both DNA strand breaks and chromosomal damages in experimental animals. Their genotoxic effects, however, do not depend only on particle size, surface modification (particle coating), and exposure route, but also on exposure duration. Currently available animal studies may suggest differing mechanisms (depending on the duration of exposure) by which living organisms react to NP contact. Nevertheless, due to considerable inconsistencies in the recent literature and the lack of standardised test methods - a reliable hazard assessment of NMs is still limited. Therefore, international organisations (e.g. NIOSH) suggest utmost caution when potential exposure of humans to NMs occurs, as long as evidence of their toxicological and genotoxic effect(s) is limited.     

Change in Bone Mass After Colles'' Fracture: A Case Report on Unique Data Collection and Long-Term Implications

The cast immobilization of a fractured limb results in a loss of bone mass; however, the long-term implications of that effect with regard to bone mineral status, particularly in other skeletal sites, are less known. The purpose of this study was to describe changes in bone mass in different skeletal sites triggered by Colles' fracture. The case is unique regarding the existence of baseline measurements taken just a few days before the fracture on all measurable skeletal sites, including the fractured radius. Therefore, it was also possible to determine whether the injury caused long-term bone loss in the affected and unaffected skeletal sites. The patient was a healthy, premenopausal Caucasian woman, in her late forties, who fractured her nondominant wrist as a result of low-impact fall on ice. The arm and the metacarpals were immobilized to the elbow for 5 wk. Bone mass measurements were performed with DPX-MD densitometer (Lunar Corp. Madison, WI) at baseline and 5, 10, 13, 21, and 52 wk postinjury. At the 5-wk measurement (on plaster removal) there was a notable increase in bone mineral density (BMD) and bone mineral content (BMC) in all sites of ulna and radius of the injured forearm (from 10 to 73%), followed by the apparent decline to or below the baseline at 10, 13, 21 and 52 wk of follow-up. Other skeletal sites were measured at 10 wk when a substantial decrease in BMD and BMC in some of the hip regions and lumbar spine was noticed; most notably in L3-L4, Ward's triangle, and femoral neck (from 2 to 8%) and remained such after 1 yr. Although this patient had a normal bone mineral status and no osteopenia detected before fracture, the trauma of radial fracture caused long-standing bone loss in fracture-prone areas-hip and spine. Because about 70% of bone strength is explained by its mineral density, the patient might be at increased risk for fracture later in life. The changes in bone mass after injury should be monitored and interpreted carefully, and more elaborate treatment of patients presenting with wrist fractures are needed to prevent any potential risk for later osteoporotic fractures in spine and hip and possible refracture of the injured extremity.