ORCID Profile
0000-0003-1529-5668
Current Organisations
University of Sydney
,
Yale University School of Medicine
,
Howard Hughes Medical Institute
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Macroeconomic Theory | Macroeconomics (incl. Monetary and Fiscal Theory) | Economic Theory | Financial Institutions (incl. Banking) |
Publisher: Proceedings of the National Academy of Sciences
Date: 07-07-2009
Abstract: Hepatic gluconeogenesis is a major contributing factor to hyperglycemia in the fasting and postprandial states in type 2 diabetes mellitus (T2DM). Because Sirtuin 1 (SirT1) induces hepatic gluconeogenesis during fasting through the induction of phosphoenolpyruvate carboxylase kinase (PEPCK), fructose-1,6-bisphosphatase (FBPase), and glucose-6-phosphatase (G6Pase) gene transcription, we hypothesized that reducing SirT1, by using an antisense oligonucleotide (ASO), would decrease fasting hyperglycemia in a rat model of T2DM. SirT1 ASO lowered both fasting glucose concentration and hepatic glucose production in the T2DM rat model. Whole body insulin sensitivity was also increased in the SirT1 ASO treated rats as reflected by a 25% increase in the glucose infusion rate required to maintain euglycemia during the hyperinsulinemic-euglycemic cl and could entirely be attributed to increased suppression of hepatic glucose production by insulin. The reduction in basal and cl ed rates of glucose production could in turn be attributed to decreased expression of PEPCK, FBPase, and G6Pase due to increased acetylation of signal transducer and activator of transcription 3 (STAT3), forkhead box O1 (FOXO1), and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), known substrates of SirT1. In addition to the effects on glucose metabolism, SirT1 ASO decreased plasma total cholesterol, which was attributed to increased cholesterol uptake and export from the liver. These results indicate that inhibition of hepatic SirT1 may be an attractive approach for treatment of T2DM.
Publisher: Cognizant, LLC
Date: 23-09-2022
DOI: 10.3727/108354222X16572285582868
Abstract: This article develops a conceptual framework and hypotheses to provide a better understanding of how traveler search behavior affects the information that firms provide in search advertising. Through an analysis of search advertising in the hotel industry, we find that firms provide significantly more price information in their search advertising to travelers whose search keywords indicate that they have prior product knowledge. This finding suggests that firms engage in tradeoffs between price information and product information in search advertising to better match tourists' preferences and needs. We also find that such tradeoffs depend on the advertiser type travel agents are more likely than hoteliers to provide price information to price-conscious travelers. The implications of our results for search engine marketing (SEM) are also discussed.
Publisher: Elsevier BV
Date: 09-2021
Publisher: Elsevier BV
Date: 09-2007
Publisher: Wiley
Date: 11-2011
Publisher: Elsevier BV
Date: 12-2009
Publisher: Springer Science and Business Media LLC
Date: 29-12-2010
Publisher: Springer Science and Business Media LLC
Date: 30-07-2008
DOI: 10.1038/NATURE07181
Publisher: American Physiological Society
Date: 12-2011
DOI: 10.1152/AJPENDO.00175.2011
Abstract: Islet damage from glucose toxicity is implicated in the pathogenesis of type 2 diabetes, but the sequence of events leading to islet cell dysfunction and hyperglycemia remains unclear. To examine the early stages of islet pathology resulting from increased basal glucose loads, normal awake rats were infused with glucose continuously for 10 days. Plasma glucose and markers of islet and liver function were monitored throughout the infusion. After initial hyperglycemia, rats adapted to the infusion and maintained euglycemia for approximately 4 days. Continued infusion led to worsening hyperglycemia in just 5% of rats after 6 days, but 69% after 8 days and 89% after 10 days, despite unchanged basal and stimulated plasma insulin and C-peptide concentrations. In contrast, plasma glucagon concentrations increased fivefold. Endogenous glucose production (EGP) was appropriately suppressed after 4 days (2.8 ± 0.7 vs. 6.1 ± 0.4 mg·kg −1 ·min −1 on day 0, P 0.001) but tripled between days 4 and 8 (9.9 ± 1.7 mg·kg −1 ·min −1 , P 0.01). Surprisingly, the increase in EGP was accompanied by increased mitochondrial phospho enolpyruvate carboxykinase expression with appropriate suppression of the cytosolic isoform. Infusion of anti-glucagon antibodies normalized plasma glucose to levels identical to those on day 4 and ∼300 mg/dl lower than controls. This improved glycemia was associated with a 60% reduction in EGP. These data support the novel concept that glucose toxicity may first manifest as α-cell dysfunction prior to any measurable deficit in insulin secretion. Such hyperglucagonemia could lead to excessive glucose production overwhelming the capacity of the β-cell to maintain glucose homeostasis.
Publisher: Wiley
Date: 08-2011
DOI: 10.1111/J.1540-5982.2011.01658.X
Abstract: Abstract This paper studies bank runs in a model with private money. We show that allowing claims on demand deposits to circulate as a medium of exchange can help prevent bank runs. In our model, there exists a unique banking equilibrium where no one demands early withdrawals of real goods and agents in need of liquidity use private money to finance consumption. With private money, the unique equilibrium not only eliminates bank runs but also improves banking efficiency. The implications of our model are consistent with the evidence from the banking history of the United States.
Publisher: Elsevier BV
Date: 03-2009
Publisher: Wiley
Date: 24-06-2021
DOI: 10.1111/JMCB.12845
Abstract: We study an economy in which money and credit serve as a means of payment and the settlement of credit requires money. The model extends recent developments in microfounded monetary theory to address the choice of payment methods and the effects of inflation. Whether a buyer uses money or credit depends on the fixed cost of credit and the inflation rate. In particular, inflation not only makes money less valuable, but also makes credit more expensive because of the delayed settlement. The model predicts that either very low inflation or very high inflation h ers the use of credit.
Publisher: Springer Science and Business Media LLC
Date: 07-2021
DOI: 10.1038/S42003-021-02279-8
Abstract: Genome-wide association studies have identified SLC16A13 as a novel susceptibility gene for type 2 diabetes. The SLC16A13 gene encodes SLC16A13/MCT13, a member of the solute carrier 16 family of monocarboxylate transporters. Despite its potential importance to diabetes development, the physiological function of SLC16A13 is unknown. Here, we validate Slc16a13 as a lactate transporter expressed at the plasma membrane and report on the effect of Slc16a13 deletion in a mouse model. We show that loss of Slc16a13 increases mitochondrial respiration in the liver, leading to reduced hepatic lipid accumulation and increased hepatic insulin sensitivity in high-fat diet fed Slc16a13 knockout mice. We propose a mechanism for improved hepatic insulin sensitivity in the context of Slc16a13 deficiency in which reduced intrahepatocellular lactate availability drives increased AMPK activation and increased mitochondrial respiration, while reducing hepatic lipid content. Slc16a13 deficiency thereby attenuates hepatic diacylglycerol-PKCε mediated insulin resistance in obese mice. Together, these data suggest that SLC16A13 is a potential target for the treatment of type 2 diabetes and non-alcoholic fatty liver disease.
Publisher: Elsevier BV
Date: 07-2011
Publisher: Elsevier BV
Date: 03-2014
Publisher: Elsevier BV
Date: 09-2009
Publisher: Springer Science and Business Media LLC
Date: 14-07-2021
Publisher: Springer Science and Business Media LLC
Date: 09-2011
DOI: 10.1038/NATURE10383
Publisher: Springer Science and Business Media LLC
Date: 23-07-2018
Publisher: The Endocrine Society
Date: 26-02-2010
DOI: 10.1210/EN.2009-0850
Abstract: The exact mechanisms through which ghrelin promotes lipogenesis are unknown. Uncoupling protein (UCP)-2 is a mitochondrial protein important in regulating reactive oxygen species however, recent research shows that it may play an important role fat metabolism. Given that ghrelin increases UCP2 mRNA in white adipose tissue, we examined whether the lipogenic actions of ghrelin are modulated by UCP2 using ucp2+/+ and ucp2−/− mice. Chronic ghrelin treatment either via osmotic minipumps or daily ip injections induced body weight gain in both ucp2+/+ and ucp2−/− mice however, body weight gain was potentiated in ucp2−/− mice. Increased body weight gain was completely due to increased body fat as a result of decreased fat oxidation in ucp2−/− mice. Ghrelin treatment of ucp2−/− mice resulted in a gene expression profile favoring lipogenesis. In a calorie-restriction model of negative energy balance, ghrelin to ucp2+/+ mice did not increase body weight however, ghrelin to ucp2−/− mice still induced body weight. These results show that UCP2 plays an important role in fat metabolism by promoting fat oxidation and restricts ghrelin-induced lipogenesis.
Publisher: Walter de Gruyter GmbH
Date: 25-01-2009
Publisher: Elsevier BV
Date: 04-2020
Publisher: Wiley
Date: 22-11-2018
Publisher: Cambridge University Press (CUP)
Date: 05-08-2016
DOI: 10.1017/S1365100516000559
Abstract: Current Population Survey (CPS) data over the period from 1994 to 2008 show that inflation has a positive effect on the residual wage dispersion. To explain this phenomenon, we introduce uncoordinated job searches into a general equilibrium monetary search framework. Our model shows that the uncoordinated job searches by unemployed workers give rise to an equilibrium, where a firm is matched with zero, one, or multiple job applicants. The ex post difference in matching probabilities generates a two-point wage dispersion among identical workers, when the Mortensen rule is implemented in the wage-determination process. In our model, inflation positively influences the wage dispersion directly through its impact on firm's real profit and indirectly through the effect of inflation that spills over from the goods market to the labor market. With reasonable parameter values, the calibrated model can account for most of the observed responses of residual wage dispersion to inflation.
Location: United States of America
Location: United States of America
Location: United States of America
Start Date: 06-2021
End Date: 06-2025
Amount: $287,304.00
Funder: Australian Research Council
View Funded ActivityStart Date: 2021
End Date: 2024
Funder: Australian Research Council
View Funded Activity