Dr. Umar

Plasma metabolomics distinguished type 1 diabetes stages. New-onset disease showed higher gut bacteria–linked 3-phenylpropionic acid and lower hypotaurine, while later-stage disease showed higher 5-methylcytosine. Ratios of phenylalanine to 3-PPA improved stage classification.

In hepcidin in pediatric type 1 diabetes, single serum hepcidin did not distinguish functional iron deficiency from normal iron status, though it was markedly low in absolute iron deficiency. The study provides iron-phenotype labeling guidance but contains no microbiome taxa or metabolite data.

This review explains how ZnT8 autoantibodies refine type 1 diabetes prediction and classification, emphasizing late-appearing epitope spreading, genotype-shaped epitope specificity, and rapid post-diagnosis decline. It also flags a candidate microbial mimicry link with Mycobacterium avium subsp. paratuberculosis.

Multi-omics profiling shows new-onset pediatric T1D features reduced butyrate and bile-acid metabolism capacity with increased LPS potential; these shifts associate with worse glycemia and inflammatory signaling and can transfer dysglycemia via FMT in mice, while butyrate is protective and LPS is harmful.

Global-childhood-type-1-diabetes-epidemiology shows rising childhood T1D incidence/prevalence but falling DALYs and mortality from 1990–2021. High-income regions carry the most cases, while Sub-Saharan Africa carries the most harm, and mortality inequality has worsened.

Serum LCN2 is a sensitive blood biomarker of active ulcerative colitis, mechanistically driven by IL-17A/IL-22/TNF-α synergy in epithelial cells. In Crohn’s disease, IL23R risk alleles associate with lower LCN2, implying genetically constrained antimicrobial responses.

This study shows fecal NGAL is a stable, high-performing stool biomarker for active IBD, comparable to fecal calprotectin, with added biological value because NGAL reflects epithelial as well as neutrophil inflammation.

This mouse study validates fecal lipocalin 2 biomarker as a highly sensitive, non-invasive stool marker that detects low-grade and severe colitis, rises within 1 day of injury, tracks spontaneous IL-10–mediated colitis severity, and declines with mucosal healing.

This study shows that IL-17/IL-22-driven lipocalin-2 shapes inflamed gut ecology by blocking enterochelin-mediated iron uptake, selecting for lipocalin-2–resistant S. Typhimurium with salmochelin (iroBCDE iroN/iroN). Lipocalin-2 thus acts as an inflammatory ecological filter.

24p3/Ngal is shown to bind iron and deliver it into renal cells via receptor-mediated uptake and acidic endosomal trafficking, regulating iron-responsive genes. In embryonic kidney, 24p3 and transferrin target different developmental cell populations, supporting stage-specific iron delivery mechanisms.

Lipocalin 2 sequestrates bacterial siderophores, restricting iron uptake by enterobactin-dependent Enterobacteriaceae. In mice, lipocalin 2 deficiency causes higher E. coli bacteremia and mortality, while bypass siderophores (ferrichrome) overcome protection and S. aureus remains unaffected.

Lipocalin-2 (LCN2/NGAL) is an inflammation-responsive protein central to microbiome–host interactions. It limits bacterial growth by binding iron-scavenging siderophores and is measurable in stool as a noninvasive marker of intestinal inflammation, including IBD.

A menthol/limonene/gingerol supplement added to standard care improved IBS/IBS+FD symptoms over 30 days versus placebo, without clear FDR-significant microbiome shifts. Fusobacterium (low abundance) showed the strongest positive correlation with symptom severity, highlighting a potential severity-associated microbiome marker.

In DSS-induced UC rats, D-limonene reduced disease severity and suppressed NF-κB-driven cytokines, COX-2/PGE2, iNOS, MMP-2/9, while improving SOD/GSH and restoring p-ERK1/2. No microbiome data were collected, but pathways align with microbe-triggered inflammation biology.

In an E. coli mouse model, lemon essential oil reduced oxidative stress, cytokines, and duodenal damage while restoring tight junction gene expression. Whole-oil LEO outperformed high-purity d-limonene at similar doses, implying multi-terpene synergy relevant to barrier-focused microbiome phenotyping.

In a mouse CDAD model, carvacrol reduced diarrhea and clinical severity while shifting the microbiome away from Proteobacteria/Enterobacteriaceae blooms and toward Lactobacillaceae/Lachnospiraceae enrichment, without markedly decreasing alpha diversity—highlighting a potential microbiome-sparing prophylactic strategy.

This review explains how plants and microbes produce terpenes and isoprenoids via MVA/MEP pathways and why their chemical diversity supports ecology, therapeutics, nutraceuticals, fragrances, and biofuels. It is microbiome-adjacent through antimicrobial and immunomodulatory bioactivity.

Terpenes and terpenoids are plant isoprenoids that can shape gut microbial ecology and intestinal barrier function. Microbiome studies of limonene, carvacrol, and menthol suggest clinically relevant, compound-specific effects that support emerging microbiome-informed nutrition and therapeutics.

This study shows hepcidin cleanly distinguishes ACD from ACD/IDA and predicts oral iron responsiveness. High hepcidin locks iron in macrophages and blocks absorption; low hepcidin restores ferroportin, absorption, and mobilization—an iron-state signature relevant to microbiome ecology.

This review explains how luminal iron availability reshapes gut microbial communities, often enriching Enterobacteriaceae and reducing Bifidobacterium/Lactobacillus, with downstream effects on SCFAs, oxidative stress, inflammation, IBD severity, and pathogen fitness. Iron route (oral vs IV) matters clinically.

This study shows that transferrin-mediated iron sequestration drives nutritional immunity in Drosophila. Toll/Imd pathways induce Tsf1, causing infection-associated hypoferremia. Tsf1 loss increases susceptibility to Pseudomonas and Mucorales, and makes pyoverdine dispensable due to excess iron.

This review on transferrin receptor 1 iron uptake explains how TfR1 imports transferrin-bound iron and how IRP/IRE, HIF, miRNAs, and trafficking pathways tightly regulate receptor levels. These host iron controls indirectly shape microbiome ecology by governing iron availability that selects for iron-scavenging microbes.

Cytochrome c-549 cyclic photophosphorylation in Anacystis nidulans is strongly dependent on redox poise, peaking at ~50% reduced cofactor. Inhibitors implicate plastoquinone and cytochrome f, while CO selectively blocks the cytochrome c-549 pathway.

This review explains how human transferrin binds and releases iron, how receptor-mediated cycling controls delivery, and how transferrin variants and post-translational modifications can disrupt iron handling. These mechanisms shape nutritional immunity and influence transferrin and microbiome interactions via microbial iron competition.

Transferrin is the plasma iron-binding protein that delivers iron to tissues while restricting microbial access to this essential nutrient. Through transferrin receptors and nutritional immunity, transferrin links iron homeostasis to immune defense and microbiome ecology.

This review explains how inflammation drives anemia via hepcidin-mediated iron sequestration, impaired iron absorption, and suppressed erythropoiesis, framing AI as “nutritional immunity.” It highlights diagnostic pitfalls with coexisting iron deficiency and summarizes current and emerging hepcidin-targeted treatments.

This minireview synthesizes how gut dysbiosis and hepcidin-driven iron mismanagement reinforce hepatic inflammation and stellate-cell activation in fibrosis, highlighting SCFAs, LPS/TLR4 signaling, and microbiota effects on intestinal iron transport as actionable pathways.

This study shows that IL-6-dependent hepcidin induction is a dominant host response to both bacterial (S. pneumoniae) and viral (influenza PR8) pneumonia, and to several TLR ligands, with IL-6 knockout or antibody blockade largely abolishing hepcidin upregulation.

This mechanistic study shows IL-6 directly induces hepcidin transcription via STAT3 binding to a defined promoter element (CE9) in hepatocyte-like cells, explaining a key pathway for anemia of inflammation and offering a framework for integrating inflammatory iron restriction into microbiome-related clinical interpretation.

This study showed that hepcidin ferroportin internalization is driven by direct binding of hepcidin to ferroportin, triggering lysosomal degradation and blocking iron export. The mechanism explains inflammatory hypoferremia and iron-loading disorders, although no microbiome taxa were assessed.

This review explains how hepcidin and ferroportin govern systemic iron absorption, recycling, and inflammation-driven iron restriction. It reframes iron overload and anemia syndromes as disorders of hepcidin deficiency or excess, with direct implications for diagnosis, therapy, and microbial iron ecology.

Hepcidin urinary antimicrobial peptide is a liver-derived, disulfide-rich peptide found in urine that kills select bacteria and inhibits fungal growth. It is primarily expressed in the liver, exists as multiple processed isoforms, and shows salt-sensitive antimicrobial activity relevant to host–microbe interactions.

Hepcidin is a liver peptide hormone that controls systemic iron by binding ferroportin and limiting iron export. Inflammation and microbial signals can increase hepcidin, promoting iron restriction and anemia of inflammation. Hepcidin is clinically useful for microbiome-informed evaluation of iron disorders.

LEAP-1 is a newly discovered, liver-expressed antimicrobial peptide found in human plasma. It is a 25–amino acid, four–disulfide peptide with strongest activity against Gram-positive bacteria and yeast, suggesting a liver-linked innate immune mechanism that may shape microbiome composition.

This study shows that aflatoxin B1 detoxification can be achieved by Bacillus amyloliquefaciens WF2020, mainly via thermostable extracellular enzymes, while also suppressing Aspergillus flavus aflatoxin gene expression and eliminating toxin production. Safety assays supported low toxicity.

Aflatoxin B1 gut microbiota metabolism is disrupted in F344 rats, with dose-dependent loss of fecal metabolites, reduced SCFAs and polyamines, and major pathway derangements (amino acids, pantothenate/CoA, pyruvate). Eight indicator metabolites form a predictive fecal signature of microbiota-dependent metabolic toxicity.

A mechanistic review of how aflatoxin B1 (a fungal toxin) is activated by CYP3A4 into a DNA-reactive epoxide and detoxified mainly by GSTs, especially GSTM1-1. Epoxide hydrolase contributes little. Chemoprevention may work by inhibiting P450s and inducing GSTs.

This review synthesizes evidence that aflatoxins and fumonisins in staple foods drive major health risks, especially aflatoxin-related liver cancer amplified by HBV. It highlights biomarkers, mechanistic pathways, emerging non-cancer outcomes, and practical prevention strategies to reduce exposure globally.

This review links aflatoxin growth impairment through biomarker-supported evidence, especially in West African children during weaning. Dose–response associations with stunting and reduced height velocity suggest aflatoxin contributes to growth faltering, potentially via immune modulation and gut barrier disruption.

This mouse study evaluated acute safety of soluble allomelanin and engineered melanized E. coli Nissle. Neither caused weight loss or intestinal inflammation, and targeted microbial markers remained stable, while melanized E. coli Nissle rapidly colonized the gut within 3 hours and persisted for 24 hours.

Aflatoxin is a carcinogenic foodborne mycotoxin that damages the liver through DNA-reactive metabolites. It also disrupts gut microbiome metabolism and gut–liver signaling, potentially contributing to inflammation and barrier dysfunction. Microbiome medicine integrates exposure biomarkers with microbial and metabolic signatures for risk assessment.

This mouse study evaluated acute safety of soluble allomelanin and engineered melanized E. coli Nissle. Neither caused weight loss or intestinal inflammation, and targeted microbial markers remained stable, while melanized E. coli Nissle rapidly colonized the gut within 3 hours and persisted for 24 hours.

This review explains how bacteria produce melanin through DOPA, homogentisate (pyomelanin), and polyketide routes, how metals and stress regulators control pigmentation, and why melanins matter for virulence, persistence, and biotechnology.

This review explains how fungal melanin virulence in Cryptococcus neoformans enables immune evasion and persistence. In vivo melanization is supported by chemical markers, melanin-specific probes, and isolation of melanin “ghosts,” and melanization reduces susceptibility to oxidative killing and amphotericin B.

This study defines a nutrient-starvation–responsive network controlling cryptococcal melanin, centered on transcription factors Hob1, Bzp4, Usv101, and Mbs1 and upstream kinases Gsk3 and Kic1, converging on LAC1 laccase induction and pigment deposition programs.

This review explains how MC1R signaling controls eumelanin versus pheomelanin balance and how pheomelanin-biased pigmentation increases melanoma risk via oxidative stress and immune effects, including UV-independent mechanisms. No microbiome taxa or microbial pathways are reported.

This review connects microbial melanin and the microbiome to melanin’s structural diversity, measurement methods, and bioactivities. It highlights why accurate melanin classification matters and how microbial melanins may signal stress tolerance, persistence, and translational opportunities in antimicrobial and photothermal biomaterials.

Melanin is a family of biologic pigments with strong UV-absorbing and antioxidant properties. Humans use melanin for photoprotection, while many microbes use melanin to resist stress and enhance survival. In microbiome medicine, melanin can influence microbial resilience and host–microbe interactions.

This consensus statement provides reactive oxygen species measurement guidelines, emphasizing ROS chemical specificity, validated probes, orthogonal confirmation, and MS-based oxidative damage biomarkers. It warns against common artefacts (DCFH-DA, HE/MitoSOX fluorescence-only, TBARS) and stresses biomarker verification in clinical trials.

ROS in gastrointestinal inflammation are both antimicrobial signals and drivers of tissue injury. This review links NOX/DUOX and mitochondrial ROS to IBD, showing that low ROS (oxidase variants) and high ROS (dysfunction/upregulation) can each promote pathology, with microbiome ties such as Proteobacteria expansion.

In mice lacking epithelial NOX activity, the gut microbiome adapts by enriching H2O2-producing lactobacilli. This community suppresses Citrobacter rodentium virulence by downregulating LEE genes (ler/escN), conferring transmissible protection that is lost with antibiotics or Western diet.

This review explains how NOX1/DUOX2/NOX2-derived ROS—especially H₂O₂—act as microbiome-relevant signals that regulate pathogen virulence, commensal ecology, and mucosal repair, and why ROS deficiency (not just excess) can drive severe IBD phenotypes.

This review explains how free radicals drive health and disease through oxidative and reductive stress, detailing mitochondrial and hyperglycemia-linked sources and why many antioxidants fail clinically. It proposes cold atmospheric plasma as a tunable redox therapy for both degenerative and proliferative disorders.

This mini review reframes oxidative stress as a mechanistically grounded redox imbalance affecting signaling and damage, warns against nonspecific “ROS” language and total antioxidant capacity testing, and emphasizes enzymatic antioxidant defenses. It offers no direct microbiome signatures but clarifies host redox biology relevant to disease interpretation.

Reactive oxygen species (ROS) are oxygen-based molecules that act in immune defense and cellular signaling. In the gut, epithelial and immune-cell ROS shape microbial ecology and barrier function. Excess ROS contributes to oxidative stress, inflammation, and permeability changes relevant to microbiome medicine.

EDTA worsened colitis and increased colitis-associated tumors in two IBD mouse models, disrupted epithelial barrier integrity, reduced microbiome diversity, and enriched Akkermansia muciniphila and Peptostreptococcaceae—supporting EDTA as a diet-linked driver of inflammatory dysbiosis and carcinogenesis risk.

Intestinal permeability to [51Cr]EDTA in asymptomatic Crohn’s disease closely reflects subclinical inflammation. Elevated urinary excretion often occurred despite normal serum markers and low CDAI, and aligned with positive Indium-111 leukocyte scans, suggesting permeability is a sensitive indirect indicator of mild–moderate active disease.

In 52Cr-EDTA intestinal permeability in Crohns disease, urinary 52Cr-EDTA excretion correlated with fecal calprotectin and showed dysbiosis-consistent trends (lower F. prausnitzii, higher Enterobacteriaceae). This non-radioactive test may support noninvasive monitoring of subclinical activity and barrier-focused phenotyping.

EDTA increases intestinal permeability in rats, boosting absorption of neutral, basic, and acidic poorly absorbed compounds and increasing reverse flux of inulin into the lumen. Findings imply calcium-chelation loosens epithelial barriers, with implications for oral drug delivery and microbiome-related biomarker interpretation.

This review explains how tight junction proteins and signaling pathways control intestinal permeability and how cytokines, pathogens, and microbiome-derived metabolites (especially SCFAs) disrupt or restore the barrier, shaping inflammatory and systemic disease risk.

EDTA anticoagulant diagnostic sample stability is strongest for hematology, nucleic acids, and protease-labile peptides, but EDTA can cause platelet clumping/pseudothrombocytopenia, interfere with some cytokine and troponin assays, and confound electrolytes via chelation or contamination.

EDTA is a metal-binding compound used as a blood anticoagulant and food stabilizer. By binding calcium, it can influence intestinal barrier integrity, and EDTA-based permeability tests are used in gut research. Experimental data also link EDTA exposure to worsened colitis in models.

Ambient long-term organophosphorus pesticide exposure gut microbiome signatures were associated with specific genus-level shifts and predicted functional changes (cell-wall/respiration pathways, reduced B1/B6 synthesis), despite no differences in overall microbiome diversity, in an older California cohort enriched for Parkinson’s disease.

This paper uses NHANES urinary dialkyl phosphate metabolites to estimate cumulative organophosphate exposure and compares results with EPA models, finding major model conservatism and key limitations of non-specific metabolites. Clinically, DAPs are best treated as screening biomarkers and exposure confounders in microbiome studies.

This mechanistic toxicology study shows that AChE inhibition explains most acute lethality from highly toxic organophosphorus agents. Steep dose–response slopes across species and strong correlations between enzyme inhibition/reactivation kinetics and survival support AChE inhibition as the dominant mechanism.

This review explains how AChE inhibition triggers respiratory failure and SE after organophosphate exposure, and how SE drives excitotoxic, oxidative, and inflammatory brain injury. Chronic low-dose effects may occur without SE. No microbiome signatures or microbial biomarkers are reported.

Organophosphates are cholinesterase-inhibiting chemicals widely used as pesticides. Beyond neurotoxicity, evidence links chronic exposure to gut microbiome changes, barrier disruption, and metabolic effects. Microbiome medicine integrates exposure biomarkers and microbiome signatures to support personalized risk assessment.

In older adults, higher fecal calprotectin tracked with fecal calprotectin gut dysbiosis: more pro-inflammatory taxa, fewer SCFA producers, increased IL-17C/CCL19, and markedly higher indoxyl sulfate (microbiome-mediated), alongside higher BMI/obesity and more heart attack history.

This meta-analysis supports fecal calprotectin relapse prediction in adult IBD remission, identifying an optimal FC threshold of 152 µg/g with pooled sensitivity 0.72 and specificity 0.74. FC helps stratify relapse risk and can complement microbiome profiling by anchoring host inflammatory activity.

This meta-analysis shows faecal calprotectin to distinguish IBD from IBS has high pooled sensitivity (85.8%) and specificity (91.7%). It performs best as a rule-out test, with NPV 99.8% at 1% IBD prevalence. Optimal sensitivity appears at cut-offs ≤50 μg/g

Calprotectin-limits-Aspergillus-hyphal-growth by chelating zinc and manganese, restricting invasive hyphae in murine fungal keratitis. Protection is restored with recombinant calprotectin and depends on intact Zn/Mn binding, while conidial killing is calprotectin-independent. Fungal ZafA-mediated zinc uptake confers resistance and virulence.

This study shows that manganese sequestration by calprotectin is essential for maximal inhibition of multiple bacterial pathogens. A unique six-histidine Mn²⁺-binding site (enabled by the S100A9 tail) explains calprotectin’s broad antimicrobial activity and its suppression of Mn-dependent oxidative stress defenses.

Calprotectin is a neutrophil-derived protein complex measured in stool to detect intestinal inflammation. It helps distinguish IBD from functional bowel disorders and reflects mucosal immune activity that can reshape microbiome composition through antimicrobial metal sequestration.

This review summarizes evidence that fecal calprotectin is a stable, noninvasive stool biomarker reflecting neutrophilic intestinal inflammation, reliably distinguishing IBD from IBS, correlating with endoscopic/histologic activity, predicting relapse, and detecting pouchitis—useful for inflammation phenotyping alongside microbiome signatures.

What was reviewed?This review article examines how transition metals shape bacterial virulence through three interconnected processes: acquisition, limitation, and intoxication. It emphasizes the evolutionary “arms race” between microbial strategies for metal uptake and host mechanisms for nutritional immunity. The review highlights how iron, zinc, and manganese—critical cofactors for bacterial metabolism—are sequestered, restricted, or weaponized by […]

This review explains how uremic toxins in ESRD drive cardiovascular, immune, and neurological injury, emphasizing toxin classification, toxicity indices, and the superiority of hemoadsorption and advanced membranes for removing hard-to-clear solutes.

This review evaluates how clinical events during the transition from pre-ESRD to ESRD influence outcomes, highlighting fluid overload, abrupt eGFR decline, and cardiovascular stress as major determinants of early ESRD mortality.

End-stage renal disease is the irreversible loss of kidney function marked by uremic toxin accumulation, systemic complications, and the need for dialysis or transplantation. Its pathophysiology involves nephron loss, inflammation, metabolic disruption, and microbiome-derived toxins that accelerate cardiovascular and immune dysfunction.

This review explores how dietary fiber influences microbiome activity, uremic toxins, inflammation, and clinical outcomes in CKD, highlighting substantial benefits and the need for individualized, fiber-rich dietary approaches.

A synthesis of modular nephron replacement strategies, detailing organoids, iBKs, bioprinting, and scaffolds, with emphasis on vascularization challenges and hybrid system potential.

This review examines how the chronic kidney disease gut microbiome becomes dysbiotic, elevates uremic toxins, weakens the gut barrier, and accelerates renal and cardiovascular injury, highlighting therapeutic targets.

This study shows how microbiome-derived IS and PCS drive renal fibrosis by activating the renal renin–angiotensin–aldosterone system associated epithelial-to-mesenchymal transition, amplifying TGF-β/Smad signaling and EMT features, and how losartan reduces this toxin-induced injury

Early diabetes complications dramatically increased five-year dialysis risk, with severity measured by DCSI strongly predicting renal decline.

This study compared causes of death in ESRD patients between USRDS and KPSC sources, finding low concordance and highlighting limitations in mortality attribution for clinical and translational research contexts.

What was reviewed?End-stage renal disease microbiome is framed in this StatPearls narrative review as the clinical endpoint of chronic kidney disease, integrating guideline-based staging, epidemiology, complications, and management. The chapter summarizes KDIGO criteria, registry data on ESRD burden, and guidance on renal replacement preparation. Although the review does not profile gut or oral microbial taxa, […]

The KDIGO 2012 CKD guideline synthesizes global evidence to refine CKD definition, staging, prognosis, and management, emphasizing albuminuria and GFR as core predictors of progression and mortality.

This study evaluated how serum uric acid levels relate to infection outcomes in ICU patients and found that uric acid reflects renal and metabolic stress rather than prognosis.

This study analyzed how low-level heavy metal exposures influence CKD risk and identified α-klotho as a mechanistic mediator, highlighting cadmium’s nephrotoxicity and complex mixture effects.

CKD increases blood lead and cadmium concentrations while reducing urinary elimination, heightening susceptibility to heavy metal toxicity in CKD, with disproportionately greater effects in Black Americans.

Nickel exposure induces gut microbiome disorder and serum uric acid elevation by disrupting purine-degrading microbes, increasing inflammatory taxa, impairing intestinal metabolism, and elevating serum uric acid in humans and mice.

This review outlines how hyperuricemia in chronic kidney disease arises from distinct filtration and tubular reabsorption defects, driving inflammation, endothelial dysfunction, and renal decline while highlighting emerging phenotype-guided approaches to therapy.

The study demonstrates that arsenic exposure is independently associated with CKDu in central India, with CKDu and CKD patients showing heavier burdens of cadmium, lead, and chromium than healthy individuals.

This study examined chronic exposure to multiple heavy metals and found strong individual and synergistic effects on renal injury biomarkers, revealing metal–metal interactions highly relevant to environmental and microbiome-linked kidney dysfunction.

Study of chronic kidney disease microbiome resistance showing metal–antibiotic co-resistance, early-stage enrichment of Firmicutes/Proteobacteria, and progressive loss of resistance genes as CKD advances.

Serum zinc levels decreased with worsening diabetic kidney disease, especially with macroalbuminuria, linking zinc deficiency to nutritional decline, sarcopenia, oxidative stress, and potential microbiome shifts influencing disease progression.

This study links low-level heavy metal exposure to increased CKD risk and higher cadmium-associated mortality, with synergistic toxicity when both metals are elevated.

This study compared heavy metal exposure and kidney function in Korea, revealing expected nephrotoxicity in the general population but paradoxically preserved eGFR in chronically exposed vulnerable communities.

Functional gastrointestinal disorders are symptom-based gut–brain interaction syndromes with no structural lesion, involving motility, visceral sensitivity, immune activation, dysbiosis, and central processing, diagnosed using Rome IV criteria.

Type 1 diabetes is an autoimmune condition in which pancreatic β-cells are destroyed, causing insulin deficiency and hyperglycemia. It typically arises in youth and requires lifelong insulin therapy. This article provides a clinician-focused review of T1D’s causes, mechanisms, complications, diagnosis, and management, including emerging multi-omics insights.