A tale of two Sea Points: gentrification, supermarkets and food security for lower-income residents

This research is founded on the argument that food systems are (and should be) a core mandate for urban planners, particularly as food is connected to many other functions relevant for built-environment professionals. To date, city officials and built-environment professionals in South Africa have adopted a laissez-faire attitude to food systems, simply assuming that for their constituents, food security can be easily solved by supporting urban agriculture projects and allowing the private sector to open new supermarket retail outlets across a city. While the literature on food security in South Africa's poorer areas is vast, no other published South African studies have considered the ways in which inner city regeneration and commercial supermarket expansion combine to impact the food security of the urban poor. Using a case study approach, this research aims to uncover the food security implications, which arise from gentrification and the growth of the commercial supermarket sector, for middle- and low-income households in Sea Point, an inner-city neighbourhood of Cape Town. This study used techniques including interviews, photography, mapping, food-price recording, document and archival research, and direct observation. It was discovered that gentrification creates an environment where local food systems are altered by policy prescriptions and improvement projects which, in turn, enable the growth of commercial food retail and high-end food service outlets. This research shows being located close to a supermarket is no guarantee of being able to afford what's being sold, and this is important because inadequate access to good-quality food has implications for health and human development over time. The experience and knowledge gained from this research has been used to support appropriate food security policy recommendations for the City of Cape Town

Serumantikörperreaktivitäten gegen Membranproteine von Prevotella intermedia, Prevotella nigrescens und Tannerella forsythensis bei Patienten mit chronischer Parodontitis

Die Parodontitis ist eine chronische polymikrobielle Biofilminfektion. Im Verlauf der bakteriellen Kolonisation werden gegen Mikroorganismen hochspezifische Antikörper gebildet. Ziel dieser Studie war es, bei 35 Patienten mit chronischer Parodontitis mit Hilfe des Western Blots zu untersuchen, gegen welche Oberflächenantigene von Prevotella intermedia, Prevotella nigrescens und Tannerella forsythensis die Serumimmunglobuline gerichtet sind, ob eine Korrelation zwischen den Antikörperreaktivitäten und den klinischen Parametern besteht und Unterschiede zwischen Therapiebeginn (Phase I), und 6 Monate später (Phase IV) zu verzeichnen sind. Die vorliegende Arbeit hat gezeigt, dass für P.i. ein Hauptantigen bei ca. 79-kDa, für P.n. bei ca. 47-kDa und für T.f. bei 58-kDa und 68-kDa in beiden Phasen besteht. Jedoch konnte beim Vergleich der zwei Phasen keine Korrelation zwischen der Antikörperreaktivität, der Infektion und der Progredienz der klinischen Parameter festgestellt werden

The Myocyte Expression of Adiponectin Receptors and PPARδ Is Highly Coordinated and Reflects Lipid Metabolism of the Human Donors

Muscle lipid oxidation is stimulated by peroxisome proliferator-activated receptor (PPAR) δ or adiponectin receptor signalling. We studied human myocyte expression of the PPARδ and adiponectin receptor genes and their relationship to lipid parameters of the donors. The mRNA levels of the three adiponectin receptors, AdipoR1, AdipoR2, and T-cadherin, were highly interrelated (r ≥ 0.91). However, they were not associated with GPBAR1, an unrelated membrane receptor. In addition, the adiponectin receptors were positively associated with PPARδ expression (r ≥ 0.75). However, they were not associated with PPARα. Using stepwise multiple linear regression analysis, PPARδ was a significant determinant of T-cadherin (P = .0002). However, pharmacological PPARδ activation did not increase T-cadherin expression. The myocyte expression levels of AdipoR1 and T-cadherin were inversely associated with the donors' fasting plasma triglycerides (P < .03). In conclusion, myocyte expression of PPARδ and the adiponectin receptors are highly coordinated, and this might be of relevance for human lipid metabolism in vivo

Common Genetic Variation in the SERPINF1 Locus Determines Overall Adiposity, Obesity-Related Insulin Resistance, and Circulating Leptin Levels

OBJECTIVE: Pigment epithelium-derived factor (PEDF) belongs to the serpin family of peptidase inhibitors (serpin F1) and is among the most abundant glycoproteins secreted by adipocytes. In vitro and mouse in vivo data revealed PEDF as a candidate mediator of obesity-induced insulin resistance. Therefore, we assessed whether common genetic variation within the SERPINF1 locus contributes to adipose tissue-related prediabetic phenotypes in humans. SUBJECTS/METHODS: A population of 1,974 White European individuals at increased risk for type 2 diabetes was characterized by an oral glucose tolerance test with glucose and insulin measurements (1,409 leptin measurements) and genotyped for five tagging SNPs covering 100% of common genetic variation (minor allele frequency ≥ 0.05) in the SERPINF1 locus. In addition, a subgroup of 486 subjects underwent a hyperinsulinaemic-euglycaemic clamp and a subgroup of 340 magnetic resonance imaging (MRI) and spectroscopy (MRS). RESULTS: After adjustment for gender and age and Bonferroni correction for the number of SNPs tested, SNP rs12603825 revealed significant association with MRI-derived total adipose tissue mass (p = 0.0094) and fasting leptin concentrations (p = 0.0035) as well as nominal associations with bioelectrical impedance-derived percentage of body fat (p = 0.0182) and clamp-derived insulin sensitivity (p = 0.0251). The association with insulin sensitivity was completely abolished by additional adjustment for body fat (p = 0.8). Moreover, the fat mass-increasing allele of SNP rs12603825 was significantly associated with elevated fasting PEDF concentrations (p = 0.0436), and the PEDF levels were robustly and positively associated with all body fat parameters measured and with fasting leptin concentrations (p<0.0001, all). CONCLUSION: In humans at increased risk for type 2 diabetes, a functional common genetic variant in the gene locus encoding PEDF contributes to overall body adiposity, obesity-related insulin resistance, and circulating leptin levels

Insulin Promotes Glycogen Storage and Cell Proliferation in Primary Human Astrocytes

In the human brain, there are at least as many astrocytes as neurons. Astrocytes are known to modulate neuronal function in several ways. Thus, they may also contribute to cerebral insulin actions. Therefore, we examined whether primary human astrocytes are insulin-responsive and whether their metabolic functions are affected by the hormone.Commercially available Normal Human Astrocytes were grown in the recommended medium. Major players in the insulin signaling pathway were detected by real-time RT-PCR and Western blotting. Phosphorylation events were detected by phospho-specific antibodies. Glucose uptake and glycogen synthesis were assessed using radio-labeled glucose. Glycogen content was assessed by histochemistry. Lactate levels were measured enzymatically. Cell proliferation was assessed by WST-1 assay.We detected expression of key proteins for insulin signaling, such as insulin receptor β-subunit, insulin receptor substrat-1, Akt/protein kinase B and glycogen synthase kinase 3, in human astrocytes. Akt was phosphorylated and PI-3 kinase activity increased following insulin stimulation in a dose-dependent manner. Neither increased glucose uptake nor lactate secretion after insulin stimulation could be evidenced in this cell type. However, we found increased insulin-dependent glucose incorporation into glycogen. Furthermore, cell numbers increased dose-dependently upon insulin treatment.This study demonstrated that human astrocytes are insulin-responsive at the molecular level. We identified glycogen synthesis and cell proliferation as biological responses of insulin signaling in these brain cells. Hence, this cell type may contribute to the effects of insulin in the human brain