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Xiaoli, A. M.

Publications and source records attributed to Xiaoli, A. M..

5 recordsLinked to original sources

A novel subset of hepatocytes is simultaneously gluconeogenic and de novo lipogenic in the fed state and is naturally insulin resistant

It is generally accepted that hepatic gluconeogenesis, the synthesis of glucose from non-carbohydrate substrates is active in the fasted state and inactive in the fed state. In contrast, de novo lipogenesis is active in the fed state and is inactive in the fasted state. Here, we used targeted single cell RNA-seq, HCR RNA-FISH, and PrimeFlow in normal physiological mouse liver, and identified a subpopulation of periportal hepatocytes that simultaneously co-express both gluconeogenic and lipogenic genes in the fed state. Euglycemic-hyperinsulinemic clamps further demonstrated that this novel hepatocyte subpopulation is naturally insulin resistant. Spatial metabolic imaging coupled with stable isotope tracing analyses revealed individual hepatocytes that simultaneously undergo both gluconeogenesis and de novo lipogenesis. These dual-positive hepatocytes were also present in human hepatocytes from humanized mouse livers. Moreover, the number of dual-positive hepatocytes increased in high-fat diet-fed mice, suggesting a paradigm shift in our understanding of how the liver becomes insulin resistant.

molecular biology↗

Spatial hepatocyte plasticity of gluconeogenesis during the metabolic transitions between fed, fasted and starvation states

The liver acts as a master regulator of metabolic homeostasis in part by performing gluconeogenesis. This process is dysregulated in type 2 diabetes, leading to elevated hepatic glucose output. The parenchymal cells of the liver (hepatocytes) are heterogeneous, existing on an axis between the portal triad and the central vein, and perform distinct functions depending on location in the lobule. Here, using single cell analysis of hepatocytes across the liver lobule, we demonstrate that gluconeogenic gene expression (Pck1 and G6pc) is relatively low in the fed state and gradually increases first in the periportal hepatocytes during the initial fasting period. As the time of fasting progresses, pericentral hepatocyte gluconeogenic gene expression increases, and following entry into the starvation state, the pericentral hepatocytes show similar gluconeogenic gene expression to the periportal hepatocytes. Similarly, pyruvate-dependent gluconeogenic activity is approximately 10-fold higher in the periportal hepatocytes during the initial fasting state but only 1.5-fold higher in the starvation state. In parallel, starvation suppresses canonical beta-catenin signaling and modulates expression of pericentral and periportal glutamine synthetase and glutaminase, resulting in an enhanced pericentral glutamine-dependent gluconeogenesis. These findings demonstrate that hepatocyte gluconeogenic gene expression and gluconeogenic activity are highly spatially and temporally plastic across the liver lobule, underscoring the critical importance of using well-defined feeding and fasting conditions to define the basis of hepatic insulin resistance and glucose production.

molecular biology↗

Complement C3 reduces apoptosis in human cardiomyocytes

Complement C3 is a key factor in complement system. Our recently animal study found that C3 may regulate myocardial apoptosis through the intrinsic apoptosis pathway. The current work investigated if C3 regulation of apoptosis occurred in human cardiomyocytes. Our results showed that incubation of exogenous C3 reduced apoptosis in a cell culture system of human cardiomyocytes which did not inherently express C3. In addition, C3 inhibited intrinsic apoptosis pathway in a cell-free apoptosis system. Furthermore, pro-C3 was found to bind with an apoptotic factor, pro-caspase 3, in a cell-free system. Thus, we presented firsthand evidence that exogenous C3 is readily reduce apoptosis in human cardiomyocytes via interaction with the intrinsic apoptotic pathway.

cell biology↗

The regulation of liver gene expression by carbohydrates is mouse strain specific

C57BL/6J and BALB/cJ mouse strains were analyzed by deep mRNA sequencing of the liver in the fasted state and following ingestion of standard laboratory mouse chow supplemented with plain drinking water or water containing 20% glucose, sucrose or fructose. Supplementation with these carbohydrates induced unique extents and temporal changes in gene expressions in a strain specific manner. Fructose and sucrose stimulated gene changes peaked at 3 h postprandial, whereas glucose effects peaked at 12 h postprandial in C57BL/6J mice and at 6 h postprandial in BABL/cJ mice. Network analyses revealed that fructose changed genes were primarily involved in lipid metabolism and were more complex in C57BL/6J than in BALB/cJ mice. These data demonstrate that there are qualitative and quantitative differences in the normal physiological responses of the liver between these two strains of mice and C57BL/6J is more sensitive to sugar intake than BALB/cJ.

genomics↗

The genome of North American beaver provides insights into the mechanisms of its longevity and cancer resistance

The North American beaver (Castor canadensis) is an exceptionally long-lived and cancer-resistant rodent species, and thus an excellent model organism for comparative genomic studies of longevity. Here, we utilize a significantly improved beaver genome assembly to assess evolutionary changes in gene coding sequences, copy number, and expression. We found that the beaver Aldh1a1, a stem cell marker gene encoding an enzyme required for detoxification of ethanol and aldehydes, is expanded (~10 copies vs. two in mouse and one in human). We also show that the beaver cells are more resistant to ethanol, and beaver liver extracts show higher ability to metabolize aldehydes than the mouse samples. Furthermore, Hpgd, a tumor suppressor gene, is uniquely duplicated in the beaver among rodents. Our evolutionary analysis identified beaver genes under positive selection which are associated with tumor suppression and longevity. Genes involved in lipid metabolism show positive selection signals, changes in copy number and altered gene expression in beavers. Several genes involved in DNA repair showed a higher expression in beavers which is consistent with the trend observed in other long-lived mammals. In summary, we identified several genes that likely contribute to beaver longevity and cancer resistance, including increased ability to detoxify aldehydes, enhanced tumor suppression and DNA repair, and altered lipid metabolism.

genomics↗