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Article: Editorial: Developing strategies to improve diabetes management in college-going young adults.

Saikia, Mridusmita / Lassi, Zohra S / McCall, Anthony L

2024 Volume 15, Page(s) 1402133

MeSH term(s)	Humans ; Young Adult ; Diabetes Mellitus/therapy ; Students ; Universities ; Disease Management
Language	English
Publishing date	2024-04-10
Publishing country	Switzerland
Document type	Editorial ; Introductory Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2024.1402133
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Article: Alpha-cell paracrine signaling in the regulation of beta-cell insulin secretion.

Holter, Marlena M / Saikia, Mridusmita / Cummings, Bethany P

Frontiers in endocrinology

2022 Volume 13, Page(s) 934775

Abstract: As an incretin hormone, glucagon-like peptide 1 (GLP-1) lowers blood glucose levels by enhancing glucose-stimulated insulin secretion from pancreatic beta-cells. Therapies targeting the GLP-1 receptor (GLP-1R) use the classical incretin model as a ... ...

Abstract	As an incretin hormone, glucagon-like peptide 1 (GLP-1) lowers blood glucose levels by enhancing glucose-stimulated insulin secretion from pancreatic beta-cells. Therapies targeting the GLP-1 receptor (GLP-1R) use the classical incretin model as a physiological framework in which GLP-1 secreted from enteroendocrine L-cells acts on the beta-cell GLP-1R. However, this model has come into question, as evidence demonstrating local, intra-islet GLP-1 production has advanced the competing hypothesis that the incretin activity of GLP-1 may reflect paracrine signaling of GLP-1 from alpha-cells on GLP-1Rs on beta-cells. Additionally, recent studies suggest that alpha-cell-derived glucagon can serve as an additional, albeit less potent, ligand for the beta-cell GLP-1R, thereby expanding the role of alpha-cells beyond that of a counterregulatory cell type. Efforts to understand the role of the alpha-cell in the regulation of islet function have revealed both transcriptional and functional heterogeneity within the alpha-cell population. Further analysis of this heterogeneity suggests that functionally distinct alpha-cell subpopulations display alterations in islet hormone profile. Thus, the role of the alpha-cell in glucose homeostasis has evolved in recent years, such that alpha-cell to beta-cell communication now presents a critical axis regulating the functional capacity of beta-cells. Herein, we describe and integrate recent advances in our understanding of the impact of alpha-cell paracrine signaling on insulin secretory dynamics and how this intra-islet crosstalk more broadly contributes to whole-body glucose regulation in health and under metabolic stress. Moreover, we explore how these conceptual changes in our understanding of intra-islet GLP-1 biology may impact our understanding of the mechanisms of incretin-based therapeutics.
MeSH term(s)	Glucagon-Like Peptide 1/metabolism ; Glucose/metabolism ; Incretins/metabolism ; Insulin/metabolism ; Insulin Secretion ; Paracrine Communication
Chemical Substances	Incretins ; Insulin ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-07-26
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2022.934775
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Article ; Online: The Many Virtues of tRNA-derived Stress-induced RNAs (tiRNAs): Discovering Novel Mechanisms of Stress Response and Effect on Human Health.

Saikia, Mridusmita / Hatzoglou, Maria

The Journal of biological chemistry

2015 Volume 290, Issue 50, Page(s) 29761–29768

Abstract: In mammalian cells, mature tRNAs are cleaved by stress-activated ribonuclease angiogenin to generate 5'- and 3'-tRNA halves: a novel class of small non-coding RNAs of 30-40 nucleotides in length. The biogenesis and biological functions of tRNA halves are ...

Abstract	In mammalian cells, mature tRNAs are cleaved by stress-activated ribonuclease angiogenin to generate 5'- and 3'-tRNA halves: a novel class of small non-coding RNAs of 30-40 nucleotides in length. The biogenesis and biological functions of tRNA halves are emerging areas of research. This review will discuss the most recent findings on: (i) the mechanism and regulation of their biogenesis, (ii) their mechanism of action (we will specifically discuss their role in the protein synthesis inhibition and the intrinsic pathway of apoptosis), and (iii) their effects on the human physiology and disease conditions.
MeSH term(s)	Humans ; Hydrolysis ; Neurodegenerative Diseases/genetics ; Neurons/metabolism ; RNA, Transfer/genetics ; Stress, Physiological
Chemical Substances	RNA, Transfer (9014-25-9)
Language	English
Publishing date	2015-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.R115.694661
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Article ; Online: 14-3-3-zeta mediates GLP-1 receptor agonist action to alter α cell proglucagon processing.

Holter, Marlena M / Phuong, Daryl J / Lee, Isaac / Saikia, Mridusmita / Weikert, Lisa / Fountain, Samantha / Anderson, Elizabeth T / Fu, Qin / Zhang, Sheng / Sloop, Kyle W / Cummings, Bethany P

Science advances

2022 Volume 8, Issue 29, Page(s) eabn3773

Abstract: Recent studies demonstrate that α cells contribute to glucose-stimulated insulin secretion (GSIS). Glucagon-like peptide-1 receptor (GLP-1R) agonists potently potentiate GSIS, making these drugs useful for diabetes treatment. However, the role of α and β ...

Abstract	Recent studies demonstrate that α cells contribute to glucose-stimulated insulin secretion (GSIS). Glucagon-like peptide-1 receptor (GLP-1R) agonists potently potentiate GSIS, making these drugs useful for diabetes treatment. However, the role of α and β cell paracrine interactions in the effects of GLP-1R agonists is undefined. We previously found that increased β cell GLP-1R signaling activates α cell GLP-1 expression. Here, we characterized the bidirectional paracrine cross-talk by which α and β cells communicate to mediate the effects of the GLP-1R agonist, liraglutide. We find that the effect of liraglutide to enhance GSIS is blunted by α cell ablation in male mice. Furthermore, the effect of β cell GLP-1R signaling to activate α cell GLP-1 is mediated by a secreted protein factor that is regulated by the signaling protein, 14-3-3-zeta, in mouse and human islets. These data refine our understanding of GLP-1 pharmacology and identify 14-3-3-zeta as a potential target to enhance α cell GLP-1 production.
Language	English
Publishing date	2022-07-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abn3773
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Article: Congenital hemihyperplasia with hemipigmentation: A rare presentation.

Arora, Major Vishal / Choubey, Major Sanjay / Saikia, Mridusmita / Fotedar, Shivani

Journal of anaesthesiology, clinical pharmacology

2015 Volume 31, Issue 2, Page(s) 253–255

Abstract: Hemihyperplasia is a heterogenous group of disorders characterized by asymmetric limb growth. Confusion regarding their classification and ascertainment into various syndromes still exists. Subtle, asymmetric variation of the unilateral structures of the ...

Abstract	Hemihyperplasia is a heterogenous group of disorders characterized by asymmetric limb growth. Confusion regarding their classification and ascertainment into various syndromes still exists. Subtle, asymmetric variation of the unilateral structures of the head, face, trunk or extremities may occur in the general population in the absence of any local lesion or condition.
Language	English
Publishing date	2015-05-06
Publishing country	India
Document type	Case Reports
ZDB-ID	1401760-x
ISSN	0970-9185
ISSN	0970-9185
DOI	10.4103/0970-9185.155161
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Article ; Online: Codon optimality controls differential mRNA translation during amino acid starvation.

Saikia, Mridusmita / Wang, Xiaoyun / Mao, Yuanhui / Wan, Ji / Pan, Tao / Qian, Shu-Bing

RNA (New York, N.Y.)

2016 Volume 22, Issue 11, Page(s) 1719–1727

Abstract: It is common wisdom that codon usage bias has evolved in the selection for efficient translation, in which highly expressed genes are encoded predominantly by optimal codons. However, a growing body of evidence suggests regulatory roles for non-optimal ... ...

Abstract	It is common wisdom that codon usage bias has evolved in the selection for efficient translation, in which highly expressed genes are encoded predominantly by optimal codons. However, a growing body of evidence suggests regulatory roles for non-optimal codons in translation dynamics. Here we report that in mammalian cells, non-optimal codons play a critical role in promoting selective mRNA translation during amino acid starvation. During starvation, in contrast to genes encoding ribosomal proteins whose translation is highly sensitive to amino acid deprivation, translation of genes involved in the cellular protein degradation pathways remains unaffected. We found that these two gene groups bear different codon composition, with non-optimal codons being highly enriched in genes encoding the ubiquitin-proteasome system. Supporting the selective tRNA charging model originally proposed in Escherichia coli, we demonstrated that tRNA isoacceptors decoding rare codons are maintained in translating ribosomes under amino acid starvation. Finally, using luciferase reporters fused with endogenous gene-derived sequences, we show that codon optimality contributes to differential mRNA translation in response to amino acid starvation. These results highlight the physiological significance of codon usage bias in cellular adaptation to stress.
MeSH term(s)	Amino Acids/metabolism ; Codon ; Protein Biosynthesis ; RNA, Messenger/genetics ; RNA, Transfer/genetics ; Ribosomes/metabolism
Chemical Substances	Amino Acids ; Codon ; RNA, Messenger ; RNA, Transfer (9014-25-9)
Language	English
Publishing date	2016-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1241540-6
ISSN	1469-9001 ; 1355-8382
ISSN (online)	1469-9001
ISSN	1355-8382
DOI	10.1261/rna.058180.116
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Zs.A 4777: Show issues

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Article ; Online: GLP-1 receptor signaling increases PCSK1 and β cell features in human α cells.

Saikia, Mridusmita / Holter, Marlena M / Donahue, Leanne R / Lee, Isaac S / Zheng, Qiaonan C / Wise, Journey L / Todero, Jenna E / Phuong, Daryl J / Garibay, Darline / Coch, Reilly / Sloop, Kyle W / Garcia-Ocana, Adolfo / Danko, Charles G / Cummings, Bethany P

JCI insight

2021 Volume 6, Issue 3

Abstract: Glucagon-like peptide-1 (GLP-1) is an incretin hormone that potentiates glucose-stimulated insulin secretion. GLP-1 is classically produced by gut L cells; however, under certain circumstances α cells can express the prohormone convertase required for ... ...

Abstract	Glucagon-like peptide-1 (GLP-1) is an incretin hormone that potentiates glucose-stimulated insulin secretion. GLP-1 is classically produced by gut L cells; however, under certain circumstances α cells can express the prohormone convertase required for proglucagon processing to GLP-1, prohormone convertase 1/3 (PC1/3), and can produce GLP-1. However, the mechanisms through which this occurs are poorly defined. Understanding the mechanisms by which α cell PC1/3 expression can be activated may reveal new targets for diabetes treatment. Here, we demonstrate that the GLP-1 receptor (GLP-1R) agonist, liraglutide, increased α cell GLP-1 expression in a β cell GLP-1R-dependent manner. We demonstrate that this effect of liraglutide was translationally relevant in human islets through application of a new scRNA-seq technology, DART-Seq. We found that the effect of liraglutide to increase α cell PC1/3 mRNA expression occurred in a subcluster of α cells and was associated with increased expression of other β cell-like genes, which we confirmed by IHC. Finally, we found that the effect of liraglutide to increase bihormonal insulin+ glucagon+ cells was mediated by the β cell GLP-1R in mice. Together, our data validate a high-sensitivity method for scRNA-seq in human islets and identify a potentially novel GLP-1-mediated pathway regulating human α cell function.
MeSH term(s)	Animals ; Female ; Gene Knockdown Techniques ; Glucagon-Like Peptide-1 Receptor/agonists ; Glucagon-Like Peptide-1 Receptor/deficiency ; Glucagon-Like Peptide-1 Receptor/genetics ; Glucagon-Like Peptide-1 Receptor/metabolism ; Glucagon-Secreting Cells/drug effects ; Glucagon-Secreting Cells/metabolism ; Humans ; Hypoglycemic Agents/pharmacology ; In Vitro Techniques ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Liraglutide/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Proprotein Convertase 1/metabolism ; RNA-Seq ; Signal Transduction
Chemical Substances	GLP1R protein, human ; Glp1r protein, mouse ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents ; Liraglutide (839I73S42A) ; PCSK1 protein, human (EC 3.4.21.93) ; Proprotein Convertase 1 (EC 3.4.21.93)
Language	English
Publishing date	2021-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.141851
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Article ; Online: Hepatocyte p53 ablation induces metabolic dysregulation that is corrected by food restriction and vertical sleeve gastrectomy in mice.

Holter, Marlena M / Garibay, Darline / Lee, Seon A / Saikia, Mridusmita / McGavigan, Anne K / Ngyuen, Lily / Moore, Elizabeth S / Daugherity, Erin / Cohen, Paul / Kelly, Kathleen / Weiss, Robert S / Cummings, Bethany P

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 34, Issue 1, Page(s) 1846–1858

Abstract: P53 has been implicated in the pathogenesis of obesity and diabetes; however, the mechanisms and tissue sites of action are incompletely defined. Therefore, we investigated the role of hepatocyte p53 in metabolic homeostasis using a hepatocyte-specific ... ...

Abstract	P53 has been implicated in the pathogenesis of obesity and diabetes; however, the mechanisms and tissue sites of action are incompletely defined. Therefore, we investigated the role of hepatocyte p53 in metabolic homeostasis using a hepatocyte-specific p53 knockout mouse model. To gain further mechanistic insight, we studied mice under two complementary conditions of restricted weight gain: vertical sleeve gastrectomy (VSG) or food restriction. VSG or sham surgery was performed in high-fat diet-fed male hepatocyte-specific p53 wild-type and knockout littermates. Sham-operated mice were fed ad libitum or food restricted to match their body weight to VSG-operated mice. Hepatocyte-specific p53 ablation in sham-operated ad libitum-fed mice impaired glucose homeostasis, increased body weight, and decreased energy expenditure without changing food intake. The metabolic deficits induced by hepatocyte-specific p53 ablation were corrected, in part by food restriction, and completely by VSG. Unlike food restriction, VSG corrected the effect of hepatocyte p53 ablation to lower energy expenditure, resulting in a greater improvement in glucose homeostasis compared with food restricted mice. These data reveal an important new role for hepatocyte p53 in the regulation of energy expenditure and body weight and suggest that VSG can improve alterations in energetics associated with p53 dysregulation.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Body Weight/physiology ; Caloric Restriction/methods ; Diet, High-Fat/adverse effects ; Eating/physiology ; Energy Metabolism/physiology ; Food ; Gastrectomy/methods ; Hepatocytes/metabolism ; Homeostasis/physiology ; Male ; Metabolic Diseases/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/metabolism ; Tumor Suppressor Protein p53/metabolism ; Weight Gain/physiology ; Weight Loss
Chemical Substances	Blood Glucose ; Trp53 protein, mouse ; Tumor Suppressor Protein p53
Language	English
Publishing date	2019-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201902214R
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Elevated circulating Th2 but not group 2 innate lymphoid cell responses characterize canine atopic dermatitis.

Früh, Simon P / Saikia, Mridusmita / Eule, Jeremy / Mazulis, Christina A / Miller, Julia E / Cowulich, Joby M / Oyesola, Oyebola O / Webb, Lauren M / Peng, Seth A / Cubitt, Rebecca L / Danko, Charles G / Miller, William H / Tait Wojno, Elia D

Veterinary immunology and immunopathology

2020 Volume 221, Page(s) 110015

Abstract: Atopic dermatitis (AD) is an allergic skin disease that causes significant morbidity and affects multiple species. AD is highly prevalent in companion dogs, and the clinical management of the disease remains challenging. An improved understanding of the ... ...

Abstract	Atopic dermatitis (AD) is an allergic skin disease that causes significant morbidity and affects multiple species. AD is highly prevalent in companion dogs, and the clinical management of the disease remains challenging. An improved understanding of the immunologic and genetic pathways that lead to disease could inform the development of novel treatments. In allergic humans and mouse models of AD, the disease is associated with Th2 and group 2 innate lymphoid cell (ILC2) activation that drives type 2 inflammation. Type 2 inflammation also appears to be associated with AD in dogs, but gaps remain in our understanding of how key type 2-associated cell types such as canine Th2 cells and ILC2s contribute to the pathogenesis of canine AD. Here, we describe previously uncharacterized canine ILC2-like cells and Th2 cells ex vivo that produced type 2 cytokines and expressed the transcription factor Gata3. Increased circulating Th2 cells were associated with chronic canine AD. Single-cell RNA sequencing revealed a unique gene expression signature in T cells in dogs with AD. These findings underline the importance of pro-allergic Th2 cells in orchestrating AD and provide new methods and pathways that can inform the development of improved therapies.
MeSH term(s)	Animals ; Blood Cells/immunology ; Dermatitis, Atopic/immunology ; Dermatitis, Atopic/veterinary ; Dog Diseases/immunology ; Dogs ; Female ; Immunity, Innate ; Inflammation ; Lymphocytes/classification ; Lymphocytes/immunology ; Male ; Sequence Analysis, RNA ; Single-Cell Analysis ; Th2 Cells/immunology
Language	English
Publishing date	2020-01-24
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	754160-0
ISSN	1873-2534 ; 0165-2427
ISSN (online)	1873-2534
ISSN	0165-2427
DOI	10.1016/j.vetimm.2020.110015
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Article ; Online: Simultaneous multiplexed amplicon sequencing and transcriptome profiling in single cells.

Saikia, Mridusmita / Burnham, Philip / Keshavjee, Sara H / Wang, Michael F Z / Heyang, Michael / Moral-Lopez, Pablo / Hinchman, Meleana M / Danko, Charles G / Parker, John S L / De Vlaminck, Iwijn

Nature methods

2018 Volume 16, Issue 1, Page(s) 59–62

Abstract: We describe droplet-assisted RNA targeting by single-cell sequencing (DART-seq), a versatile technology that enables multiplexed amplicon sequencing and transcriptome profiling in single cells. We applied DART-seq to simultaneously characterize the non-A- ...

Abstract	We describe droplet-assisted RNA targeting by single-cell sequencing (DART-seq), a versatile technology that enables multiplexed amplicon sequencing and transcriptome profiling in single cells. We applied DART-seq to simultaneously characterize the non-A-tailed transcripts of a segmented dsRNA virus and the transcriptome of the infected cell. In addition, we used DART-seq to simultaneously determine the natively paired, variable region heavy and light chain amplicons and the transcriptome of B lymphocytes.
MeSH term(s)	Animals ; B-Lymphocytes/metabolism ; Cell Line ; Gene Expression Profiling ; Mice ; Real-Time Polymerase Chain Reaction ; Reverse Transcription ; Single-Cell Analysis/methods ; Transcriptome
Language	English
Publishing date	2018-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2169522-2
ISSN	1548-7105 ; 1548-7091
ISSN (online)	1548-7105
ISSN	1548-7091
DOI	10.1038/s41592-018-0259-9
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