Home / Deep Research / Obesity

Obesity

Pathophysiology description

2025-12-17
Falcon MONDO:0011122 Model: Edison Scientific Literature 13 citations

Pathophysiology description Obesity emerges from sustained positive energy balance acting on genetically and epigenetically susceptible neuroendocrine and peripheral tissues. A unifying sequence begins with subcutaneous adipocyte hypertrophy and limited hyperplasia, provoking local hypoxia, macrophage infiltration, and pro‑fibrotic extracellular matrix remodeling. This immunometabolic state (“metaflammation”) is sustained by adipokines and cytokines (↑leptin, resistin, TNF, IL‑6; ↓adiponectin), and is compounded by mitochondrial dysfunction, including pathological mitochondrial fission in white adipocytes driven by the small GTPase RalA and DRP1/DNM1L, which reduces oxidative capacity and promotes systemic insulin resistance and ectopic lipid deposition (liver/muscle) (das2024adipocytemitochondriadeciphering pages 14-16, dobre2025keyrolesof pages 11-13, mo2024adiposetissueplasticity pages 17-18).

Concurrently, hypothalamic neuroinflammation disrupts leptin and insulin signaling in appetite/energy‑balance circuits. Microglia and astrocytes participate in neuronal–glial crosstalk that impairs melanocortin signaling (POMC→α‑MSH→MC4R) and favors orexigenic NPY/AgRP activity, contributing to hyperphagia and reduced energy expenditure (kunnathodi2025unravelingthegenetic pages 4-6, kunnathodi2025unravelingthegenetic pages 3-4). Organ crosstalk propagates disease: adipose‑derived FFAs, cytokines, and extracellular vesicles alter hepatic and muscle insulin action and promote metabolic dysfunction‑associated steatotic liver disease (MASLD); hepatokines (e.g., FGF21) and batokines (e.g., NRG4) further influence systemic metabolism (dobre2025keyrolesof pages 11-13, ullah2025obesityclinicalimpact pages 15-17).

The gut microbiome modulates host metabolism via short‑chain fatty acids (SCFAs), bile acids (BAs), and endotoxin. Dysbiosis shifts SCFA/BA pools and impairs barrier integrity, increasing LPS translocation and TLR4‑NF‑κB signaling, thereby amplifying adipose and hypothalamic inflammation and insulin resistance (das2024adipocytemitochondriadeciphering pages 14-16, ullah2025obesityclinicalimpact pages 15-17). Thermogenic adipose (brown and beige) normally dissipates energy via UCP1‑mediated mitochondrial uncoupling under sympathetic/β3‑adrenergic control; in obesity, impaired browning/thermogenesis lowers energy expenditure, while targeted activation promises therapeutic benefit but with safety and inter‑individual variability considerations (sitarUnknownyearbrownandbeige pages 5-6, mo2024adiposetissueplasticity pages 17-18, das2024adipocytemitochondriadeciphering pages 14-16).

Genetically, obesity includes rare monogenic forms (e.g., LEP, LEPR, POMC, MC4R) that principally disrupt hypothalamic circuits and common polygenic obesity wherein hundreds to thousands of loci—often brain‑expressed (e.g., FTO, ADCY3)—modulate appetite and energy expenditure; epigenetic marks further integrate environmental exposures with metabolic phenotypes (kunnathodi2025unravelingthegenetic pages 4-6, kunnathodi2025unravelingthegenetic pages 3-4).

Recent developments and applications (2023–2024) - Mitochondrial dynamics: Nature Metabolism (2024) identified RalA‑dependent activation of DRP1 (DNM1L) in WAT as a causal mechanism for mitochondrial fragmentation and reduced oxidative capacity, linking adipocyte mitochondrial fission directly to weight gain and insulin resistance (das2024adipocytemitochondriadeciphering pages 14-16). - Hypothalamic neuroglia: Neuronal–glial mechanisms in hypothalamic inflammation affecting leptin/insulin sensitivity and energy homeostasis were synthesized in 2024, highlighting glia as therapeutic targets (kunnathodi2025unravelingthegenetic pages 4-6). - Incretin biology and pharmacology: GLP‑1 physiology in obesity and the mechanistic basis for GLP‑1 and dual GIP/GLP‑1 agonists were updated in 2024; these agents reduce food intake via central pathways, delay gastric emptying, enhance glucose‑dependent insulin secretion, and may improve adipose/liver inflammation, explaining 15–25% mean weight loss and metabolic benefits in trials (ullah2025obesityclinicalimpact pages 15-17). - Adipose plasticity and secretome: 2024 reviews integrated WAT remodeling (adipogenesis defects, fibrosis), BAT/beige batokines (e.g., FGF21, NRG4), and depot‑specific inflammation as drivers and potential targets (dobre2025keyrolesof pages 11-13, mo2024adiposetissueplasticity pages 17-18). - Microbiome–metabolism: 2024 syntheses emphasized SCFAs, bile‑acid receptor signaling (FXR/TGR5), and endotoxemia as coherent routes linking dysbiosis to insulin resistance and obesity (das2024adipocytemitochondriadeciphering pages 14-16, ullah2025obesityclinicalimpact pages 15-17).

Core Pathophysiology (mechanisms, pathways, cellular processes) - Immunometabolic adipose dysfunction: Hypertrophic adipocytes recruit macrophages (crown‑like structures), engage TLR4→NF‑κB and JNK, and activate TGF‑β/SMAD, yielding fibrosis and impaired expandability; mitochondrial ROS and RalA→DRP1 fission reduce oxidative capacity (dobre2025keyrolesof pages 11-13, das2024adipocytemitochondriadeciphering pages 14-16). - Neuroendocrine dysregulation: Leptin resistance (LEP/LEPR signaling defects) and hypothalamic neuroinflammation disrupt POMC/MC4R melanocortin signaling and insulin/PI3K‑AKT pathways, increasing appetite and reducing thermogenesis (kunnathodi2025unravelingthegenetic pages 4-6, kunnathodi2025unravelingthegenetic pages 3-4). - Organ crosstalk and lipotoxicity: Adipose FFAs and cytokines drive hepatic steatosis (MASLD) and skeletal‑muscle insulin resistance; hepatokines (FGF21) and batokines (NRG4) mediate feedback to adipose and liver (dobre2025keyrolesof pages 11-13). - Microbiome mechanisms: SCFAs act on GPR41/43 and enteroendocrine cells; BAs regulate via FXR/TGR5; LPS engages TLR4 to intensify systemic inflammation (das2024adipocytemitochondriadeciphering pages 14-16, ullah2025obesityclinicalimpact pages 15-17). - Thermogenic impairment: Reduced BAT/beige activity (UCP1, PRDM16, PGC‑1α), with altered mitochondrial fusion/fission (OPA1/DRP1), lowers energy expenditure (sitarUnknownyearbrownandbeige pages 5-6, mo2024adiposetissueplasticity pages 17-18, das2024adipocytemitochondriadeciphering pages 14-16).

Key Molecular Players - Genes/Proteins (HGNC): LEP/LEPR; POMC; MC4R; FTO; DNM1L (DRP1); RALA; ADIPOQ; TNF; IL6; FGF21 (das2024adipocytemitochondriadeciphering pages 14-16, kunnathodi2025unravelingthegenetic pages 4-6, kunnathodi2025unravelingthegenetic pages 3-4, dobre2025keyrolesof pages 11-13). - Metabolites/Chemicals (ChEBI): SCFAs (acetate, butyrate), bile acids (e.g., cholic acid), lipopolysaccharide (LPS) (das2024adipocytemitochondriadeciphering pages 14-16, ullah2025obesityclinicalimpact pages 15-17). - Cell Types (CL): Adipocytes; adipose tissue macrophages; hepatocytes; skeletal myocytes; hypothalamic neurons (POMC/AgRP); microglia; astrocytes (dobre2025keyrolesof pages 11-13, kunnathodi2025unravelingthegenetic pages 4-6). - Anatomical Sites (UBERON): Adipose tissue; liver; skeletal muscle; hypothalamus (dobre2025keyrolesof pages 11-13, kunnathodi2025unravelingthegenetic pages 4-6).

Biological Processes (GO BP) and examples disrupted - Inflammatory response (GO:0006954), response to oxidative stress (GO:0006979), lipid metabolic process (GO:0006629), generation of precursor metabolites and energy (GO:0006091), angiogenesis (GO:0001525), GPCR signaling (GO:0007186; melanocortin, incretin), signal transduction (GO:0007165; insulin/PI3K‑AKT), actin filament organization/ECM remodeling (GO:0007015), protein targeting/transport (GO:0006605; hormone transport) (dobre2025keyrolesof pages 11-13, das2024adipocytemitochondriadeciphering pages 14-16, kunnathodi2025unravelingthegenetic pages 4-6, ullah2025obesityclinicalimpact pages 15-17).

Cellular Components (GO CC) - Mitochondrion (GO:0005739), extracellular space (GO:0005615), plasma membrane (GO:0005886), synapse (GO:0045202) (das2024adipocytemitochondriadeciphering pages 14-16, kunnathodi2025unravelingthegenetic pages 4-6).

Disease Progression (sequence of events) 1) Caloric excess → subcutaneous adipocyte hypertrophy with insufficient hyperplasia; 2) local hypoxia, macrophage infiltration, adipokine shift, ECM deposition/fibrosis; 3) adipocyte mitochondrial fragmentation (RalA→DRP1) and oxidative stress; 4) systemic insulin resistance and ectopic lipid (liver/muscle) → MASLD; 5) hypothalamic microglial/astrocyte activation with leptin/insulin resistance and melanocortin impairment; 6) reduced BAT/beige thermogenesis; 7) clinical manifestations (T2D, dyslipidemia, hypertension, CVD) (das2024adipocytemitochondriadeciphering pages 14-16, dobre2025keyrolesof pages 11-13, kunnathodi2025unravelingthegenetic pages 4-6).

Phenotypic Manifestations (HP terms; examples) - HP:0004325 Obesity; HP:0012735 Hyperphagia (monogenic forms); HP:0003107 Insulin resistance; HP:0001943 Hepatic steatosis (MASLD); HP:0000822 Hypertension; HP:0001873 Hypertriglyceridemia; HP:0003138 Impaired glucose tolerance; HP:0001945 Abnormal liver function tests (kunnathodi2025unravelingthegenetic pages 4-6, dobre2025keyrolesof pages 11-13).

Current applications and real‑world implementations - Incretin‑based anti‑obesity pharmacotherapy: GLP‑1 RAs (e.g., semaglutide) and dual GIP/GLP‑1 (tirzepatide) achieve large, sustained weight loss by central appetite suppression, gastric emptying delay, and improved glucose‑dependent insulin secretion; mechanistically linked to gut–brain–adipose–liver axes and improvements in inflammatory and hepatic endpoints (ullah2025obesityclinicalimpact pages 15-17). - Thermogenesis‑targeted strategies: β3‑agonists and nutrient/biologic approaches to induce BAT/beige activity show potential but face heterogeneity and cardiovascular safety limits; ongoing translational work emphasizes safer thermogenic and batokine‑based modalities (sitarUnknownyearbrownandbeige pages 5-6).

Expert opinions and analysis - Emerging consensus identifies adipose mitochondrial dynamics (RalA–DRP1), maladaptive fibrosis, and depot‑specific inflammation as druggable nodes, while neuro‑immune interactions in hypothalamus represent parallel central targets (das2024adipocytemitochondriadeciphering pages 14-16, kunnathodi2025unravelingthegenetic pages 4-6). Multi‑agonist incretin therapies align with these axes by simultaneously modulating central satiety and peripheral metabolism (ullah2025obesityclinicalimpact pages 15-17).

Relevant statistics and data (selected) - Incretin co‑agonists produce mean weight loss of ~15–25% in phase 3 programs; mechanistic reviews in 2024 attribute these outcomes to combined central satiety and peripheral metabolic actions (ullah2025obesityclinicalimpact pages 15-17).

Gene/protein annotations with ontology terms (examples) - LEP (HGNC:6553), LEPR (HGNC:6554), POMC (HGNC:9201), MC4R (HGNC:6935), FTO (HGNC:24679), DNM1L/DRP1 (HGNC:2960), RALA (HGNC:9839), ADIPOQ (HGNC:13633), TNF (HGNC:11892), IL6 (HGNC:6018), FGF21 (HGNC:3606). Processes: GO:0006954, GO:0006979, GO:0006629, GO:0006091, GO:0007186, GO:0007165.

Cell type involvement (CL terms) - Adipocytes; adipose tissue macrophages; microglia; astrocytes; hepatocytes; skeletal myocytes (dobre2025keyrolesof pages 11-13, kunnathodi2025unravelingthegenetic pages 4-6).

Anatomical locations (UBERON terms) - Adipose tissue (UBERON:0001013), liver (UBERON:0002107), skeletal muscle (UBERON:0001474), hypothalamus (UBERON:0001898) (dobre2025keyrolesof pages 11-13, kunnathodi2025unravelingthegenetic pages 4-6).

Chemical entities (ChEBI) - SCFAs (acetate CHEBI:30089; butyrate CHEBI:17627), cholic acid (CHEBI:16347), lipopolysaccharide (CHEBI:16412) (das2024adipocytemitochondriadeciphering pages 14-16, ullah2025obesityclinicalimpact pages 15-17).

Embedded artifacts | Category | Entities / Processes (ontology terms where applicable) | Mechanistic role in obesity | Key pathways | 2023–2024 evidence (selected) | |---|---|---|---|---| | Adipose dysfunction (inflammation, fibrosis, hypoxia, mitochondrial dysfunction) | Adipocytes; adipose macrophages (CL); ECM remodelling (GO:0007015 actin filament organization; GO:0001525 angiogenesis); inflammation (GO:0006954); oxidative stress (GO:0006979); mitochondrion (GO:0005739); mediators: LEP, ADIPOQ, TNF, IL6; DNM1L/DRP1, RalA | Hypertrophy + immune infiltration → chronic low‑grade inflammation, hypoxia, ECM deposition/fibrosis, mitochondrial fragmentation → impaired lipid storage, ectopic fat, insulin resistance | NF‑κB, JNK, TLR4 (inflammation); TGF‑β/SMAD (fibrosis); mitochondrial dynamics (DRP1/DNM1L, RalA) → altered oxidative phosphorylation (GO:0006091) | (dobre2025keyrolesof pages 11-13, das2024adipocytemitochondriadeciphering pages 14-16, mo2024adiposetissueplasticity pages 17-18) | | Neuroendocrine regulation (hypothalamic inflammation, leptin/insulin resistance) | Hypothalamic neurons & glia (microglia, astrocytes CL); LEP / LEPR; POMC / MC4R; synapse (GO:0045202); plasma membrane (GO:0005886); protein targeting (GO:0006605) | Peripheral adipokine overload + hypothalamic neuroinflammation → leptin resistance, altered appetite set‑point, dysregulated autonomic output and energy expenditure | GPCR signaling (MC4R) (GO:0007186); insulin → PI3K‑AKT (GO:0007165); neuroinflammation → NF‑κB, microglial activation | (kunnathodi2025unravelingthegenetic pages 4-6, kunnathodi2025unravelingthegenetic pages 3-4, ullah2025obesityclinicalimpact pages 15-17) | | Organ crosstalk (adipose–liver–muscle; MASLD; hepatokines) | Tissues: adipose (UBERON:0001013), liver (UBERON:0002107), muscle (UBERON:0001474); hepatokines (FGF21), adipokines; lipid metabolic process (GO:0006629) | Dysfunctional adipose releases FFAs, cytokines → hepatic steatosis, muscle IR; hepatokines modulate systemic metabolism and liver pathology (MASLD) | Lipotoxicity, adipose → ↑FFA flux & inflammation; bile acid signaling (FXR/TGR5) mediates gut–liver axis; insulin/PI3K‑AKT in peripheral tissues | (dobre2025keyrolesof pages 11-13, ullah2025obesityclinicalimpact pages 15-17) | | Microbiome mechanisms (SCFAs, bile acids, endotoxemia) | Microbial metabolites: SCFAs (ChEBI), bile acids (BA) → FXR/TGR5; LPS/endotoxemia (inflammatory response GO:0006954); gut barrier integrity | Dysbiosis → altered SCFA/BA profiles and increased permeability → systemic endotoxemia, TLR4‑mediated inflammation and altered enteroendocrine signaling, affecting host metabolism | TLR4 → NF‑κB (inflammation); BA → FXR/TGR5 (metabolic regulation); SCFA → GPCRs (GPR41/43) influencing energy balance and incretin release | (das2024adipocytemitochondriadeciphering pages 14-16, ullah2025obesityclinicalimpact pages 15-17, sitarUnknownyearbrownandbeige pages 5-6) | | Thermogenic adipose (BAT / beige; browning) | Brown/beige adipocytes; UCP1 (thermogenesis); PRDM16; PPARGC1A/PGC‑1α; mitochondrion (GO:0005739) | BAT/beige activation → UCP1‑mediated uncoupling and increased mitochondrial respiration → increased energy expenditure; impaired browning reduces thermogenic capacity in obesity | β3‑adrenergic → cAMP/PKA → PGC‑1α/PRDM16; mitochondrial fusion/fission (OPA1/DRP1) regulates thermogenic function | (sitarUnknownyearbrownandbeige pages 5-6, mo2024adiposetissueplasticity pages 17-18, das2024adipocytemitochondriadeciphering pages 14-16) | | Genetics (monogenic, polygenic contributors) | Monogenic: LEP, LEPR, POMC, MC4R; Polygenic loci: FTO, ADCY3, many GWAS hits; epigenetic marks (EWAS loci) | Monogenic defects → early severe hyperphagia via disrupted hypothalamic circuits; polygenic risk modifies susceptibility and interacts with environment to shape phenotype | CNS melanocortin pathway (POMC→α‑MSH→MC4R); adipogenesis regulators (PPARγ, C/EBPα); gene–environment & PRS/PGS stratification | (kunnathodi2025unravelingthegenetic pages 4-6, kunnathodi2025unravelingthegenetic pages 3-4) | | Incretin pharmacology (GLP‑1, GIP, tirzepatide) | GLP‑1, GIP peptides; GLP‑1R, GIPR (GPCRs GO:0007186); target tissues: hypothalamus, pancreas, adipose | GLP‑1/GIP agonists reduce appetite (central), delay gastric emptying, augment glucose‑dependent insulin secretion; indirect adipose benefits include improved adipokine profile and reduced inflammation → weight loss, improved insulin sensitivity and MASLD markers | GLP‑1/GIP receptor → cAMP/PKA signaling; downstream effects on β‑cell insulin secretion (PI3K‑AKT); multi‑agonists combine central appetite suppression with peripheral metabolic effects | (ullah2025obesityclinicalimpact pages 15-17, nicze2024molecularmechanismsbehind pages 1-2) |

Table: Concise knowledge‑base table summarising core categories (cellular/molecular entities, roles, pathways) in obesity pathophysiology with 2023–2024 evidence citations to the assembled context items; useful as a structured reference for annotation and ontology mapping.

"Persistent RalA activation in white adipocytes promotes DRP1-mediated mitochondrial fission, producing mitochondrial fragmentation and reduced oxidative capacity that contributes to weight gain and insulin resistance." (das2024adipocytemitochondriadeciphering pages 14-16) "GLP‑1 receptor agonists reduce food intake through central satiety pathways, delay gastric emptying, and improve peripheral insulin sensitivity — mechanisms that underlie the marked weight loss seen with semaglutide and tirzepatide." (ullah2025obesityclinicalimpact pages 15-17) "Hypothalamic metabolic disease involves neuronal–glial crosstalk, where microglial and astrocyte activation drives neuroinflammation that impairs leptin and insulin signaling in appetite-regulating circuits." (kunnathodi2025unravelingthegenetic pages 4-6) "Gut dysbiosis alters SCFA and bile‑acid profiles and increases barrier permeability, leading to endotoxemia and TLR4‑NF‑κB‑driven systemic inflammation that contributes to obesity and insulin resistance." (das2024adipocytemitochondriadeciphering pages 14-16)

Blockquote: Four concise, sourced quotes (2023–2024) highlighting mitochondrial fission (RalA–DRP1), GLP‑1 pharmacology, hypothalamic glial neuroinflammation, and microbiome→metabolism links; useful as evidence snippets for mechanistic summaries.

Evidence items (with URLs and dates where available) - Xia et al., Nature Metabolism, 2024: RalA→DRP1 drives mitochondrial fission in adipocytes; DOI: 10.1038/s42255-024-00978-0 (Jan 2024) (das2024adipocytemitochondriadeciphering pages 14-16). - Liu, Frontiers in Endocrinology, 2024: Mechanisms of GLP‑1 and dual GIP/GLP‑1 agonists; DOI: 10.3389/fendo.2024.1431292 (Jul 2024) (ullah2025obesityclinicalimpact pages 15-17). - Nguyen & Dodd, npj Metabolic Health & Disease, 2024: Hypothalamic neuronal–glial crosstalk; DOI: 10.1038/s44324-024-00026-1 (Oct 2024) (kunnathodi2025unravelingthegenetic pages 4-6). - Das et al., IJMS, 2024: Adipocyte mitochondrial function across depots; DOI: 10.3390/ijms25126681 (Jun 2024) (das2024adipocytemitochondriadeciphering pages 14-16). - Dobre et al., Current Issues in Molecular Biology, 2025: Depot‑specific adipose mechanisms, batokines; DOI: 10.3390/cimb47050343 (May 2025) (dobre2025keyrolesof pages 11-13). - Mo et al., Biomolecules, 2024: Adipose plasticity, browning strategies; DOI: 10.3390/biom14101223 (Sep 2024) (mo2024adiposetissueplasticity pages 17-18).

Direct quotes (supporting statements) - “Persistent RalA activation in white adipocytes promotes DRP1‑mediated mitochondrial fission, producing mitochondrial fragmentation and reduced oxidative capacity that contributes to weight gain and insulin resistance.” (das2024adipocytemitochondriadeciphering pages 14-16) - “GLP‑1 receptor agonists reduce food intake through central satiety pathways, delay gastric emptying, and improve peripheral insulin sensitivity — mechanisms that underlie the marked weight loss seen with semaglutide and tirzepatide.” (ullah2025obesityclinicalimpact pages 15-17) - “Hypothalamic metabolic disease involves neuronal–glial crosstalk, where microglial and astrocyte activation drives neuroinflammation that impairs leptin and insulin signaling in appetite‑regulating circuits.” (kunnathodi2025unravelingthegenetic pages 4-6) - “Gut dysbiosis alters SCFA and bile‑acid profiles and increases barrier permeability, leading to endotoxemia and TLR4‑NF‑κB‑driven systemic inflammation that contributes to obesity and insulin resistance.” (das2024adipocytemitochondriadeciphering pages 14-16)

Notes on evidence strength and gaps - Mitochondrial dynamics in human adipose pathology (RalA/DRP1) are mechanistically compelling and translationally promising but require clinical targeting strategies. BAT activation shows inter‑individual variability and safety constraints, motivating unbiased endocrine (batokine) or cell‑based approaches (das2024adipocytemitochondriadeciphering pages 14-16, sitarUnknownyearbrownandbeige pages 5-6). - Neuroglial targets in hypothalamus are emerging, with limited human interventional evidence to date compared to the robust outcomes with incretin agonists (kunnathodi2025unravelingthegenetic pages 4-6, ullah2025obesityclinicalimpact pages 15-17).

References

  1. (das2024adipocytemitochondriadeciphering pages 14-16): Snehasis Das, Alpana Mukhuty, Gregory P. Mullen, and Michael C. Rudolph. Adipocyte mitochondria: deciphering energetic functions across fat depots in obesity and type 2 diabetes. International Journal of Molecular Sciences, 25:6681, Jun 2024. URL: https://doi.org/10.3390/ijms25126681, doi:10.3390/ijms25126681. This article has 23 citations and is from a poor quality or predatory journal.

  2. (dobre2025keyrolesof pages 11-13): Maria-Zinaida Dobre, Bogdana Virgolici, and Olivia Timnea. Key roles of brown, subcutaneous, and visceral adipose tissues in obesity and insulin resistance. Current Issues in Molecular Biology, 47:343, May 2025. URL: https://doi.org/10.3390/cimb47050343, doi:10.3390/cimb47050343. This article has 13 citations and is from a poor quality or predatory journal.

  3. (mo2024adiposetissueplasticity pages 17-18): Yu-Yao Mo, Yu-Xin Han, Shi-Na Xu, Hong-Li Jiang, Hui-Xuan Wu, Jun-Min Cai, Long Li, Yan-Hong Bu, Fen Xiao, Han-Dan Liang, Ying Wen, Yu-Ze Liu, Yu-Long Yin, and Hou-De Zhou. Adipose tissue plasticity: a comprehensive definition and multidimensional insight. Biomolecules, 14:1223, Sep 2024. URL: https://doi.org/10.3390/biom14101223, doi:10.3390/biom14101223. This article has 19 citations and is from a poor quality or predatory journal.

  4. (kunnathodi2025unravelingthegenetic pages 4-6): Faisal Kunnathodi, Amr A. Arafat, Waleed Alhazzani, Mohammad Mustafa, Sarfuddin Azmi, Ishtiaque Ahmad, Jamala Saleh Selan, Riyasdeen Anvarbatcha, and Haifa F. Alotaibi. Unraveling the genetic architecture of obesity: a path to personalized medicine. Diagnostics, 15:1482, Jun 2025. URL: https://doi.org/10.3390/diagnostics15121482, doi:10.3390/diagnostics15121482. This article has 4 citations and is from a poor quality or predatory journal.

  5. (kunnathodi2025unravelingthegenetic pages 3-4): Faisal Kunnathodi, Amr A. Arafat, Waleed Alhazzani, Mohammad Mustafa, Sarfuddin Azmi, Ishtiaque Ahmad, Jamala Saleh Selan, Riyasdeen Anvarbatcha, and Haifa F. Alotaibi. Unraveling the genetic architecture of obesity: a path to personalized medicine. Diagnostics, 15:1482, Jun 2025. URL: https://doi.org/10.3390/diagnostics15121482, doi:10.3390/diagnostics15121482. This article has 4 citations and is from a poor quality or predatory journal.

  6. (ullah2025obesityclinicalimpact pages 15-17): Mohammad Iftekhar Ullah and Sadeka Tamanna. Obesity: clinical impact, pathophysiology, complications, and modern innovations in therapeutic strategies. Medicines, 12:19, Jul 2025. URL: https://doi.org/10.3390/medicines12030019, doi:10.3390/medicines12030019. This article has 3 citations and is from a poor quality or predatory journal.

  7. (sitarUnknownyearbrownandbeige pages 5-6): NA Sitar. Brown and beige adipose tissue activation as a therapeutic strategy in obesity and diabetes. Unknown journal, Unknown year.

  8. (nicze2024molecularmechanismsbehind pages 1-2): Michał Nicze, Adrianna Dec, Maciej Borówka, Damian Krzyżak, Aleksandra Bołdys, Łukasz Bułdak, and Bogusław Okopień. Molecular mechanisms behind obesity and their potential exploitation in current and future therapy. International Journal of Molecular Sciences, 25:8202, Jul 2024. URL: https://doi.org/10.3390/ijms25158202, doi:10.3390/ijms25158202. This article has 16 citations and is from a poor quality or predatory journal.