A bone grease processing station at the Mitchell Prehistoric Indian Village: archaeological evidence for the exploitation of bone fats

© Association for Environmental Archaeology 2015. Author's accepted manuscript version deposited in accordance with SHERPA RoMEO guidelines. The definitive version is available at http://www.maneyonline.com/doi/abs/10.1179/1749631414Y.0000000035.Recent excavations at the Mitchell Prehistoric Indian Village, an Initial Middle Missouri site in Mitchell, South Dakota have revealed a large, clay-lined feature filled with fractured and fragmented bison bones. Fracture and fragmentation analysis, along with taphonomic evidence, suggests that the bones preserved within the feature represent evidence of prehistoric bone marrow and bone grease exploitation. Further, the character of the feature suggests that it served as a bone grease processing station. Bone fat exploitation is an activity that is frequently cited as a causal explanation for the nature of many fractured and fragmented bone assemblages in prehistory, and zooarchaeological assemblages have frequently been studied as evidence of bone fat exploitation. The Mitchell example provides some of the first direct, in-situ archaeological evidence of a bone grease processing feature, and this interpretation is sustained by substantial analytical evidence suggesting bone fat exploitation. This new evidence provides a clearer concept of the nature of bone fat exploitation in prehistory as well as an indication of the scale and degree to which bone grease exploitation occurred at the Mitchell site. Finally, this research demonstrates the importance of careful zooarchaeological and taphonomic analysis for the interpretation of both artifactual remains as well as archaeological features

Country-specific birth weight and length in type 1 diabetes high-risk HLA genotypes in combination with prenatal characteristics

Objective:To examine the relationship between high-risk human leukocyte antigen (HLA) genotypes for type 1 diabetes and birth size in combination with prenatal characteristics in different countries.Study Design:Four high-risk HLA genotypes were enrolled in the Environmental determinants of Diabetes in the Young study newborn babies from the general population in Finland, Germany, Sweden and the United States. Stepwise regression analyses were used to adjust for country, parental physical characteristics and environmental factors during pregnancy.Result:Regression analyses did not reveal differences in birth size between the four type 1 diabetes high-risk HLA genotypes. Compared with DQ 4/8 in each country, (1) DQ 2/2 children were heavier in the United States (P=0.028) mostly explained however, by parental weight; (2) DQ 2/8 (P=0.023) and DQ 8/8 (P=0.046) children were longer in Sweden independent of parents height and as well as (3) in the United States for DQ 2/8 (P=0.023), but again dependent on parental height.Conclusion:Children born with type 1 diabetes high-risk HLA genotypes have comparable birth size. Longitudinal follow-up of these children should reveal whether birth size differences between countries contribute to the risk for islet autoimmunity and type 1 diabetes.Journal of Perinatology advance online publication, 28 April 2011; doi:10.1038/jp.2011.26

The human gut microbiome in early-onset type 1 diabetes from the TEDDY study

Type 1 diabetes (T1D) is an autoimmune disease that targets pancreatic islet beta cells and incorporates genetic and environmental factors(1), including complex genetic elements(2), patient exposures(3) and the gut microbiome(4). Viral infections(5) and broader gut dysbioses(6) have been identified as potential causes or contributing factors; however, human studies have not yet identified microbial compositional or functional triggers that are predictive of islet autoimmunity or T1D. Here we analyse 10,913 metagenomes in stool samples from 783 mostly white, non-Hispanic children. The samples were collected monthly from three months of age until the clinical end point (islet autoimmunity or T1D) in the The Environmental Determinants of Diabetes in the Young (TEDDY) study, to characterize the natural history of the early gut microbiome in connection to islet autoimmunity, T1D diagnosis, and other common early life events such as antibiotic treatments and probiotics. The microbiomes of control children contained more genes that were related to fermentation and the biosynthesis of short-chain fatty acids, but these were not consistently associated with particular taxa across geographically diverse clinical centres, suggesting that microbial factors associated with T1D are taxonomically diffuse but functionally more coherent. When we investigated the broader establishment and development of the infant microbiome, both taxonomic and functional profiles were dynamic and highly individualized, and dominated in the first year of life by one of three largely exclusive Bifidobacterium species (B. bifidum, B. breve or B. longum) or by the phylum Proteobacteria. In particular, the strain-specific carriage of genes for the utilization of human milk oligosaccharide within a subset of B. longum was present specifically in breast-fed infants. These analyses of TEDDY gut metagenomes provide, to our knowledge, the largest and most detailed longitudinal functional profile of the developing gut microbiome in relation to islet autoimmunity, T1D and other early childhood events. Together with existing evidence from human cohorts(7,8) and a T1D mouse model(9), these data support the protective effects of short-chain fatty acids in early-onset human T1D

Gut Microbiota, Probiotics and Diabetes

Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes