Archeota, Fall 2018

This is the Fall 2018 issue of Archeota, the official publication of the SJSU SAASChttps://scholarworks.sjsu.edu/saasc_archeota/1008/thumbnail.jp

Loans and Leaving: Migration and the Expansion of Microcredit in Cambodia

Over the last decade, the expansion of microfinance institutions (MFIs) has dramatically shifted the availability of credit across the developing world. This recent development provides an opportunity to examine the relationship between household labor migration and access to and use of formal credit. Both theories of migration and the expectations of formal credit providers have suggested that labor migration and credit are substitute solutions to the demand for capital in the developing world, with the implication that greater access to formal financial services may stem migration out of rural places. Using household survey data from Cambodia, an MFI-saturated country, we find that households using formal credit and households with greater access to formal credit are more likely to have labor migrants than households without access. This association persists across size of loan, purpose of loan, remittances behavior, and for domestic migrations. These findings complicate our understanding of the relationship between credit and migration, and call for a greater recognition of the importance of context in framing migration behavior

MnTBAP treatment alters insulin-stimulated PKB phosphorylation but not content in EWAT from mice fed a HFD.

<p>Mice were fed a LFD or HFD for 5 months and then treated with or without MnTBAP (10 mg/kg) daily for 5 weeks. At 15 min following an intraperitoneal injection of insulin (2 U/Kg), EWAT was excised and rapidly frozen in liquid nitrogen for subsequent Western blot experiments. <b>(A)</b> Representative PKB immunoblots for pThr³⁰⁸ and pSer⁴⁷³ PKB as well as total PKB-α and PKB-β isoforms. α-tubulin was used as a loading control. Quantification of <b>(B)</b> pThr³⁰⁸ PKB, <b>(C)</b> pSer³⁰⁸ PKB, <b>(D)</b> PKB-α and <b>(E)</b> PKB-β content, each normalized to α-tubulin. *, Denotes statistically significant difference from HFD-Vehicle. ⁺, Denotes statistically significant difference from LFD-MnTBAP. N = 5–6 mice per group.</p

MnTBAP treatment reduces body weight and adipose tissue mass in mice fed a LFD or HFD.

<p>Mice were fed a LFD or HFD for 5 months and then treated with or without MnTBAP (10 mg/kg) daily for 5 weeks. <b>(A)</b> Fed-state body weights at different treatment durations. <b>(B)</b> Fasted body weights before and after MnTBAP or vehicle treatments. <b>(C)</b> Epididymal white adipose tissue (EWAT) mass. *, Denotes statistically significant difference from respective vehicle-treated mice. ⁺, Denotes statistically significant difference from respective LFD mice. N = 5–6 mice per group.</p

MnTBAP treatment improves insulin-assisted glucose tolerance (IAGT) in mice fed a HFD.

<p>Mice were simultaneously injected with 2.0 U/Kg insulin and 2.0 g/Kg glucose and blood glucose values were assessed at baseline and 20, 40, and 60 min following the injection (Panels A) and the area under the IAGT curve was calculated (Panels B). *, Denotes statistically significant difference from HFD-Vehicle. ⁺, Denotes statistically significant difference from LFD-Vehicle mice. N = 7–14 mice per group.</p

MnTBAP treatment increase insulin-stimulated PKB phosphorylation and content in muscles from mice fed a HFD.

<p>Mice were fed a LFD or HFD for 5 months and then treated with or without MnTBAP (10 mg/kg) daily for 5 weeks. At 15 min following an intraperitoneal injection of insulin (2 U/Kg), quadriceps muscles were excised and rapidly frozen in liquid nitrogen for subsequent Western blot analyses. <b>(A)</b> Representative PKB immunoblots for pThr³⁰⁸ and pSer⁴⁷³ PKB as well as total PKB-α and PKB-β isoforms. GAPDH was used as a loading control. Quantification of <b>(B)</b> pThr³⁰⁸ PKB, <b>(C)</b> pSer³⁰⁸ PKB, <b>(D)</b> PKB-α and <b>(E)</b> PKB-β content, each normalized to GAPDH. *, Denotes statistically significant difference from HFD-Vehicle. N = 5–6 mice per group.</p

The HO-1 inhibitor SnMP does not block MnTBAP’s ability to reduce body weight, adipose tissue mass, and caloric intake in mice fed HFD.

<p>Mice were fed a LFD or HFD for 5 months and then treated with MnTBAP (10 mg/kg) alone or in combination with SnMP (20 mg/Kg) daily for 5 weeks. <b>(A)</b> Fed-state body weights at different treatment durations. <b>(B)</b> Epididymal white adipose tissue (EWAT) mass. (C) Caloric intake was assessed at various time points of MnTBAP or MnTBAP+SnMP treatment in mice previously fed a LFD or HFD for 5 months. *, Denotes statistically significant difference from LFD vehicle-treated mice. ⁺, Denotes statistically significant difference from respective LFD mice. N = 5–6 mice per group.</p

MnTBAP treatment reduces caloric intake in mice fed a HFD.

<p><b>(A)</b> Caloric intake was assessed at various time points of MnTBAP treatment in mice previously fed a LFD or HFD for 5 months. <b>(B)</b> Correlation between the change in body weight and the change in caloric intake from pre-treatment to post-treatment. *, Denotes statistically significant difference from HFD-Vehicle. ⁺, Denotes statistically significant difference from respective LFD mice. P-value for post-hoc analysis for LFD-Vehicle vs. HFD-Vehicle mice: Day 9, P = 0.057; Day 17, P = 0.085. N = 6–8 mice per group.</p