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Article ; Online: GP73 links SARS-CoV-2 infection with dysglycaemia.

Coate, Katie C

Nature metabolism

2022 Volume 4, Issue 1, Page(s) 9–10

MeSH term(s)	Biomarkers ; Blood Glucose ; COVID-19/complications ; COVID-19/virology ; Disease Susceptibility ; Glucose/metabolism ; Glucose Metabolism Disorders/diagnosis ; Glucose Metabolism Disorders/etiology ; Glucose Metabolism Disorders/metabolism ; Host-Pathogen Interactions ; Humans ; Liver/metabolism ; Liver/pathology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; SARS-CoV-2
Chemical Substances	Biomarkers ; Blood Glucose ; GOLM1 protein, human ; Membrane Proteins ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-01-07
Publishing country	Germany
Document type	Lecture ; Research Support, N.I.H., Extramural
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-021-00511-7
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Article ; Online: Integration of metabolic flux with hepatic glucagon signaling and gene expression profiles in the conscious dog.

Coate, Katie C / Ramnanan, Christopher J / Smith, Marta / Winnick, Jason J / Kraft, Guillaume / Irimia-Dominguez, Jose / Farmer, Ben / Donahue, E Patrick / Roach, Peter J / Cherrington, Alan D / Edgerton, Dale S

American journal of physiology. Endocrinology and metabolism

2024 Volume 326, Issue 4, Page(s) E428–E442

Abstract: Glucagon rapidly and profoundly stimulates hepatic glucose production (HGP), but for reasons that are unclear, this effect normally wanes after a few hours, despite sustained plasma glucagon levels. This study characterized the time course of glucagon- ... ...

Abstract	Glucagon rapidly and profoundly stimulates hepatic glucose production (HGP), but for reasons that are unclear, this effect normally wanes after a few hours, despite sustained plasma glucagon levels. This study characterized the time course of glucagon-mediated molecular events and their relevance to metabolic flux in the livers of conscious dogs. Glucagon was either infused into the hepato-portal vein at a sixfold basal rate in the presence of somatostatin and basal insulin, or it was maintained at a basal level in control studies. In one control group, glucose remained at basal, whereas in the other, glucose was infused to match the hyperglycemia that occurred in the hyperglucagonemic group. Elevated glucagon caused a rapid (30 min) and largely sustained increase in hepatic cAMP over 4 h, a continued elevation in glucose-6-phosphate (G6P), and activation and deactivation of glycogen phosphorylase and synthase activities, respectively. Net hepatic glycogenolysis increased rapidly, peaking at 15 min due to activation of the cAMP/PKA pathway, then slowly returned to baseline over the next 3 h in line with allosteric inhibition by glucose and G6P. Glucagon's stimulatory effect on HGP was sustained relative to the hyperglycemic control group due to continued PKA activation. Hepatic gluconeogenic flux did not increase due to the lack of glucagon's effect on substrate supply to the liver. Global gene expression profiling highlighted glucagon-regulated activation of genes involved in cellular respiration, metabolic processes, and signaling, as well as downregulation of genes involved in extracellular matrix assembly and development.
MeSH term(s)	Humans ; Dogs ; Animals ; Glucagon/metabolism ; Insulin/metabolism ; Transcriptome ; Glucose/metabolism ; Liver/metabolism ; Gluconeogenesis/genetics ; Blood Glucose/metabolism
Chemical Substances	Glucagon (9007-92-5) ; Insulin ; Glucose (IY9XDZ35W2) ; Blood Glucose
Language	English
Publishing date	2024-02-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00316.2023
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Article ; Online: Profound Sensitivity of the Liver to the Direct Effect of Insulin Allows Peripheral Insulin Delivery to Normalize Hepatic but Not Muscle Glucose Uptake in the Healthy Dog.

Kraft, Guillaume / Coate, Katie C / Smith, Marta / Farmer, Ben / Scott, Melanie / Hastings, Jon / Cherrington, Alan D / Edgerton, Dale S

Diabetes

2022 Volume 72, Issue 2, Page(s) 196–209

Abstract: Endogenous insulin secretion is a key regulator of postprandial hepatic glucose metabolism, but this process is dysregulated in diabetes. Subcutaneous insulin delivery alters normal insulin distribution, causing relative hepatic insulin deficiency and ... ...

Abstract	Endogenous insulin secretion is a key regulator of postprandial hepatic glucose metabolism, but this process is dysregulated in diabetes. Subcutaneous insulin delivery alters normal insulin distribution, causing relative hepatic insulin deficiency and peripheral hyperinsulinemia, a major risk factor for metabolic disease. Our aim was to determine whether insulin's direct effect on the liver is preeminent even when insulin is given into a peripheral vein. Postprandial-like conditions were created (hyperinsulinemia, hyperglycemia, and a positive portal vein to arterial glucose gradient) in healthy dogs. Peripheral (leg vein) insulin infusion elevated arterial and hepatic levels 8.0-fold and 2.8-fold, respectively. In one group, insulin's full effects were allowed. In another, insulin's indirect hepatic effects were blocked with the infusion of triglyceride, glucagon, and inhibitors of brain insulin action (intracerebroventricular) to prevent decreases in plasma free fatty acids and glucagon, while blocking increased hypothalamic insulin signaling. Despite peripheral insulin delivery the liver retained its full ability to store glucose, even when insulin's peripheral effects were blocked, whereas muscle glucose uptake markedly increased, creating an aberrant distribution of glucose disposal between liver and muscle. Thus, the healthy liver's striking sensitivity to direct insulin action can overcome the effect of relative hepatic insulin deficiency, whereas excess insulin in the periphery produces metabolic abnormalities in nonhepatic tissues.
MeSH term(s)	Animals ; Dogs ; Blood Glucose/metabolism ; Glucagon/metabolism ; Glucose/metabolism ; Hyperinsulinism/drug therapy ; Hyperinsulinism/metabolism ; Insulin/pharmacology ; Liver/drug effects ; Liver/metabolism
Chemical Substances	Blood Glucose ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2) ; Insulin
Language	English
Publishing date	2022-10-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db22-0471
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Article: Integration of metabolic flux with hepatic glucagon signaling and gene expression profiles in the conscious dog.

Coate, Katie C / Ramnanan, Christopher J / Smith, Marta / Winnick, Jason J / Kraft, Guillaume / Irimia, Jose M / Farmer, Ben / Donahue, Patrick / Roach, Peter J / Cherrington, Alan D / Edgerton, Dale S

bioRxiv : the preprint server for biology

2023

Abstract: Glucagon rapidly and profoundly simulates hepatic glucose production (HGP), but for reasons which are unclear, this effect normally wanes after a few hours, despite sustained plasma glucagon levels. This study characterized the time course and relevance ( ...

Abstract	Glucagon rapidly and profoundly simulates hepatic glucose production (HGP), but for reasons which are unclear, this effect normally wanes after a few hours, despite sustained plasma glucagon levels. This study characterized the time course and relevance (to metabolic flux) of glucagon mediated molecular events in the livers of conscious dogs. Glucagon was either infused into the hepato-portal vein at a 6-fold basal rate in the presence of somatostatin and basal insulin, or it was maintained at a basal level in control studies. In one control group glucose remained at basal while in the other glucose was infused to match the hyperglycemia that occurred in the hyperglucagonemic group. Elevated glucagon caused a rapid (30 min) but only partially sustained increase in hepatic cAMP over 4h, a continued elevation in G6P, and activation and deactivation of glycogen phosphorylase and synthase activities, respectively. Net hepatic glycogenolysis and HGP increased rapidly, peaking at 30 min, then returned to baseline over the next 3h (although glucagons stimulatory effect on HGP was sustained relative to the hyperglycemic control group). Hepatic gluconeogenic flux did not increase due to lack of glucagon effect on substrate supply to the liver. Global gene expression profiling highlighted glucagon-regulated activation of genes involved in cellular respiration, metabolic processes, and signaling, and downregulation of genes involved in extracellular matrix assembly and development.
Language	English
Publishing date	2023-10-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.28.559999
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Article ; Online: The Importance of the Mechanisms by Which Insulin Regulates Meal-Associated Liver Glucose Uptake in the Dog.

Kraft, Guillaume / Coate, Katie C / Smith, Marta / Farmer, Ben / Scott, Melanie / Cherrington, Alan D / Edgerton, Dale S

Diabetes

2021 Volume 70, Issue 6, Page(s) 1292–1302

Abstract: Hepatic glucose uptake (HGU) is critical for maintaining normal postprandial glucose metabolism. Insulin is clearly a key regulator of HGU, but the physiologic mechanisms by which it acts have yet to be established. This study sought to determine the ... ...

Abstract	Hepatic glucose uptake (HGU) is critical for maintaining normal postprandial glucose metabolism. Insulin is clearly a key regulator of HGU, but the physiologic mechanisms by which it acts have yet to be established. This study sought to determine the mechanisms by which insulin regulates liver glucose uptake under postprandial-like conditions (hyperinsulinemia, hyperglycemia, and a positive portal vein-to-arterial glucose gradient). Portal vein insulin infusion increased hepatic insulin levels fivefold in healthy dogs. In one group (
MeSH term(s)	Animals ; Blood Glucose/drug effects ; Blood Glucose/metabolism ; Carbohydrate Metabolism/drug effects ; Dogs ; Eating/physiology ; Female ; Glucose/pharmacokinetics ; Insulin/pharmacology ; Liver/drug effects ; Liver/metabolism ; Male ; Meals/physiology ; Signal Transduction/drug effects
Chemical Substances	Blood Glucose ; Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db20-1271
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Article ; Online: Hyperaminoacidemia induces pancreatic α cell proliferation via synergism between the mTORC1 and CaSR-Gq signaling pathways.

Gong, Yulong / Yang, Bingyuan / Zhang, Dingdong / Zhang, Yue / Tang, Zihan / Yang, Liu / Coate, Katie C / Yin, Linlin / Covington, Brittney A / Patel, Ravi S / Siv, Walter A / Sellick, Katelyn / Shou, Matthew / Chang, Wenhan / Danielle Dean, E / Powers, Alvin C / Chen, Wenbiao

Nature communications

2023 Volume 14, Issue 1, Page(s) 235

Abstract: Glucagon has emerged as a key regulator of extracellular amino acid (AA) homeostasis. Insufficient glucagon signaling results in hyperaminoacidemia, which drives adaptive proliferation of glucagon-producing α cells. Aside from mammalian target of ... ...

Abstract	Glucagon has emerged as a key regulator of extracellular amino acid (AA) homeostasis. Insufficient glucagon signaling results in hyperaminoacidemia, which drives adaptive proliferation of glucagon-producing α cells. Aside from mammalian target of rapamycin complex 1 (mTORC1), the role of other AA sensors in α cell proliferation has not been described. Here, using both genders of mouse islets and glucagon receptor (gcgr)-deficient zebrafish (Danio rerio), we show α cell proliferation requires activation of the extracellular signal-regulated protein kinase (ERK1/2) by the AA-sensitive calcium sensing receptor (CaSR). Inactivation of CaSR dampened α cell proliferation, which was rescued by re-expression of CaSR or activation of Gq, but not Gi, signaling in α cells. CaSR was also unexpectedly necessary for mTORC1 activation in α cells. Furthermore, coactivation of Gq and mTORC1 induced α cell proliferation independent of hyperaminoacidemia. These results reveal another AA-sensitive mediator and identify pathways necessary and sufficient for hyperaminoacidemia-induced α cell proliferation.
MeSH term(s)	Animals ; Female ; Male ; Mice ; Calcium/metabolism ; Cell Proliferation ; Glucagon ; Glucagon-Secreting Cells/metabolism ; Receptors, Calcium-Sensing/metabolism ; Signal Transduction ; Zebrafish/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Glucagon (9007-92-5) ; Receptors, Calcium-Sensing ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2023-01-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-35705-4
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Article ; Online: A pragmatic low carbohydrate diet intervention changes neither carbohydrate consumption nor glycemia in adolescents and young adults with type 1 diabetes in a randomized trial.

Duffus, Sara H / Slaughter, James C / Cooley, William / Sharif, Navila / Rainer, Kimberly / Coate, Katie C / Jaser, Sarah S / Moore, Daniel J / Niswender, Kevin D / Gregory, Justin M

Pediatric diabetes

2022 Volume 23, Issue 7, Page(s) 1088–1100

Abstract: Objective: Despite enthusiasm for low carbohydrate diets (LCDs) among patients with type 1 diabetes (T1DM), no prospective study has investigated outcomes in adolescent T1DM. We aimed to quantify a pragmatic LCD intervention's impact on glycemia, ... ...

Abstract	Objective: Despite enthusiasm for low carbohydrate diets (LCDs) among patients with type 1 diabetes (T1DM), no prospective study has investigated outcomes in adolescent T1DM. We aimed to quantify a pragmatic LCD intervention's impact on glycemia, lipidemia, and quality of life (QOL) in adolescents with T1DM. Research design and methods: At an academic center, we randomized 39 patients with T1DM aged 13-21 years to one of three 12-week interventions: an LCD, an isocaloric standard carbohydrate diet (SCD), or general diabetes education without a prescriptive diet. Glycemic outcomes included glycosylated hemoglobin (HbA1c) and continuous glucose monitoring. Results: There were no significant differences in glycemic, lipidemic, or QOL parameters between groups at any timepoint. Median HbA1c was similar at baseline between groups and did not change appreciably (7.9%-8.4% in LCDs, 7.9%-7.9% in SCDs, and 8.2%-7.8% in controls). Change in carbohydrate consumption was minimal with only one participant reaching target carbohydrate intake. Conclusions: This pragmatic LCD intervention did not alter carbohydrate consumption or glycemia. Although this study was unable to evaluate a highly controlled LCD, it indicates that adolescents are unlikely to implement an educational LCD intervention in routine clinic settings. Thus, this approach is unlikely to effectively mitigate hyperglycemia in adolescents.
MeSH term(s)	Adolescent ; Blood Glucose ; Blood Glucose Self-Monitoring ; Diabetes Mellitus, Type 1/therapy ; Diabetes Mellitus, Type 2 ; Diet, Carbohydrate-Restricted ; Glycated Hemoglobin/analysis ; Humans ; Quality of Life ; Young Adult
Chemical Substances	Blood Glucose ; Glycated Hemoglobin A
Language	English
Publishing date	2022-09-05
Publishing country	Denmark
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1502504-4
ISSN	1399-5448 ; 1745-1426 ; 1399-543X
ISSN (online)	1399-5448
ISSN	1745-1426 ; 1399-543X
DOI	10.1111/pedi.13407
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Article: Pancreatic islet α cell function and proliferation requires the arginine transporter SLC7A2.

Spears, Erick / Stanley, Jade E / Shou, Matthew / Yin, Linlin / Li, Xuan / Dai, Chunhua / Bradley, Amber / Sellick, Katelyn / Poffenberger, Greg / Coate, Katie C / Shrestha, Shristi / Jenkins, Regina / Sloop, Kyle W / Wilson, Keith T / Attie, Alan D / Keller, Mark P / Chen, Wenbiao / Powers, Alvin C / Dean, E Danielle

bioRxiv : the preprint server for biology

2023

Abstract: Interrupting glucagon signaling decreases gluconeogenesis and the fractional extraction of amino acids by liver from blood resulting in lower glycemia. The resulting hyperaminoacidemia stimulates α cell proliferation and glucagon secretion via a liver-α ... ...

Abstract	Interrupting glucagon signaling decreases gluconeogenesis and the fractional extraction of amino acids by liver from blood resulting in lower glycemia. The resulting hyperaminoacidemia stimulates α cell proliferation and glucagon secretion via a liver-α cell axis. We hypothesized that α cells detect and respond to circulating amino acids levels via a unique amino acid transporter repertoire. We found that
Language	English
Publishing date	2023-08-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.08.10.552656
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Article ; Online: Insulin Infusion Is Linked to Increased

Gregory, Justin M / Kraft, Guillaume / Farmer, Ben / Smith, Marta S / LaNeve, David C / Williams, Phillip E / Tomasek, Kelsey / Su, Yan Ru / Wilson, Christopher S / Thompson, Mark D / Cherrington, Alan D / Coate, Katie C

Journal of the Endocrine Society

2021 Volume 5, Issue 7, Page(s) bvab088

Abstract: The purpose of this study was to assess insulin-stimulated gene expression in canine skeletal muscle with a particular focus ... ...

Abstract	The purpose of this study was to assess insulin-stimulated gene expression in canine skeletal muscle with a particular focus on
Language	English
Publishing date	2021-05-08
Publishing country	United States
Document type	Journal Article
ISSN	2472-1972
ISSN (online)	2472-1972
DOI	10.1210/jendso/bvab088
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Article ; Online: MetAP2 inhibitor treatment of high-fat and -fructose-fed dogs: impact on the response to oral glucose ingestion and a hyperinsulinemic hyperglycemic clamp.

Moore, Mary Courtney / Coate, Katie C / Scott, Melanie / Kraft, Guillaume / Vath, James E / Hughes, Thomas E / Farmer, Ben / Cherrington, Alan D

American journal of physiology. Endocrinology and metabolism

2020 Volume 318, Issue 4, Page(s) E514–E524

Abstract: We examined the methionine aminopeptidase 2 inhibitor fumagillin in dogs consuming a high-fat and -fructose diet (HFFD). In pilot studies (3 dogs that had consumed HFFD for 3 yr), 8 wk of daily treatment with fumagillin reduced food intake 29%, weight 6%, ...

Abstract	We examined the methionine aminopeptidase 2 inhibitor fumagillin in dogs consuming a high-fat and -fructose diet (HFFD). In pilot studies (3 dogs that had consumed HFFD for 3 yr), 8 wk of daily treatment with fumagillin reduced food intake 29%, weight 6%, and the glycemic excursion during an oral glucose tolerance test (OGTT) 44%. A second group of dogs consumed the HFFD for 17 wk: pretreatment (
MeSH term(s)	Aminopeptidases/antagonists & inhibitors ; Animals ; Blood Glucose/metabolism ; Body Weight/drug effects ; Cyclohexanes/pharmacology ; Diet ; Diet, High-Fat/adverse effects ; Dogs ; Eating/drug effects ; Fatty Acids, Unsaturated/pharmacology ; Fructose/adverse effects ; Glucose/metabolism ; Glucose/pharmacology ; Glucose Clamp Technique ; Glucose Tolerance Test ; Insulin Resistance ; Male ; Metalloendopeptidases/antagonists & inhibitors ; Sesquiterpenes/pharmacology
Chemical Substances	Blood Glucose ; Cyclohexanes ; Fatty Acids, Unsaturated ; Sesquiterpenes ; Fructose (30237-26-4) ; fumagillin (7OW73204U1) ; Aminopeptidases (EC 3.4.11.-) ; methionine aminopeptidase 2 (EC 3.4.11.18) ; Metalloendopeptidases (EC 3.4.24.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00451.2019
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