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Open research questions in Adipokines, Inflammation, and Metabolic Diseases

551 gap statements mined from Adipokines, Inflammation, and Metabolic Diseases papers in our 7.9M-paper local library, which holds 1,803 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

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What the literature leaves open

  • One of the main limitations of the present study is the relatively small number of normal-weight participants with metabolic syndrome compared with the overweight/obese MetS group.

    Biomarkers in Obesity-Related Metabolic Syndrome: Relationships Between LDL Subfractions, Lipid Profile, and Cardiometabolic Risk in a Slovak Population · 2026 · DOI

  • In vitro studies indicated AR downregulation as a shared disease signature and showed quercetin dose-dependently restored AR expression and cell viability, offering preliminary preclinical evidence that warrants further investigation (Graphical abstract).

    Quercetin-Androgen Receptor Axis as a Potential Molecular Basis for Achyranthis Radix Coordinated Regulation of Sarcopenia, Osteoporosis, and Obesity: An Integrated Network Pharmacology and In Vitro Validation Study · 2026 · DOI

  • Third, we evaluated a single exercise modality and duration; it remains to be determined whether different intensities, durations, or resistance training produce similar systemic effects. Second, the study included only male mice; therefore, sex-specific responses should be examined in future work.

    4-week aerobic exercise training regulates systemic macrophage polarization in obese mice · 2026 · DOI

  • Higher SII values were observed in the normoglycemic group; however, the explanation for this unexpected cross-sectional association remains uncertain.

    Systemic inflammatory indices and glucose homeostasis in children with obesity: evidence from oral glucose tolerance testing · 2026 · DOI

  • Most of the causal and mechanistic evidence, including that for EV-mediated, angiocrine, EndMT-related and lymphatic mechanisms, derives from mouse and in vitro models and remains to be validated in human adipose tissue.

    Breakdown of adipocyte-endothelial communication as a driver of adipose tissue dysfunction in obesity · 2026 · DOI

  • Several important questions arising from the present framework remain unresolved. A major priority is the identification of reliable biomarkers capable of detecting early deterioration in adipose tissue function before the development of overt metabolic complications.

    Prometheus’s Fire, Part I: The Flight of Icarus—Molecular Mechanisms Underlying Adipose Tissue Dysfunction in Obesity: From Adaptive Hyperplasia to Pathological Hypertrophy · 2026 · DOI

  • Third, a limitation of the present study is the absence of an MNT10-alone group and the restriction of Western blot analysis to the CTR, DEX, and MNT20 + DEX groups.

    Dexamethasone-Induced Insulin Resistance and Hepatic Metabolic Dysfunction: Modulatory Effects of Montelukast on SGK1-Associated Signaling and NLRP3/Leukotriene-Related Responses · 2026 · DOI

  • Given that CTRPs function in an autocrine manner and can form heteromers (Table 1), future studies should investigate the ligand-receptor axes using double- or multiple-gene mutant mice to elucidate the interdependent nature of these molecules. However, the relationships between each CTRP and these receptors have not yet been fully elucidated.

    The contribution of the CTRP family and its receptors to fibrotic diseases · 2026 · DOI

  • The investigation of macrophage-derived exosomes in human studies and further studies of biomarkers such as Gal-4, MPO, ANGPTL6, BMDM, PIEZO1, BCAAs/BCKDH phosphatase, and α2-MG may clarify the inflammatory mechanisms underlying T2D and obesity and lead to improved diagnostic, disease monitoring, and therapeutic strategies.

    Molecular Mechanisms Linking Obesity and Type 2 Diabetes: Pathogenesis, Biomarkers, and Therapeutic Potential · 2026 · DOI

  • The mechanisms and pathways by which elevated Gal-4 concentrations are associated with obesity, diabetes, and cardiovascular disease are not yet known. However, the translation of these biomarkers into clinical application will require a deeper understanding of and further research into their specific mechanisms, roles, and viability as drug targets.

    Molecular Mechanisms Linking Obesity and Type 2 Diabetes: Pathogenesis, Biomarkers, and Therapeutic Potential · 2026 · DOI

  • However, most of the existing research has focused on individual inflammatory proteins, while the role of inflammatory protein signatures associated with IR and cognition remains unexplored.

    Inflammatory protein signatures as predictors of insulin resistance and cognitive function: a one-year longitudinal study in the mPRIME cohort · 2026 · DOI

  • Adipose tissue macrophage (ATM) lipid accumulation is associated with developing obesity-related insulin resistance, yet the underlying mechanisms influencing excess lipid accumulation in ATM are not well understood.

    Siah2 is a lipid-mediated metabolic sensor in adipose tissue macrophage · 2026 · DOI

  • The contribution of the p38 MAPK activator MKK3 to adipose tissue physiology remains poorly understood. The role of MKK3 in preserving insulin responsiveness in mice and its alteration in human obesity is not well characterized.

    An Adipocyte MKK3–p38β Axis Preserves Insulin Responsiveness in Mice and Is Reciprocally Altered in Human Obesity · 2026 · DOI

  • This integrated understanding of obesity as an immunometabolic disorder underscores the need to move beyond calorie-centric paradigms.

    Metaflammation’s Role in Systemic Dysfunction in Obesity: A Comprehensive Review · 2025 · DOI

  • Future research should focus on refining diagnostic criteria, elucidating underlying mechanisms, and evaluating the impact of early, routine screening for IR in diverse populations. Further research is required to investigate the interplay between metabolic and vascular health, which will be vital for developing more effective, individualized strategies for cardiovascular risk reduction.

    Atherosclerosis and Insulin Resistance: Is There a Link Between Them? · 2025 · DOI

  • Future research should focus on developing precision immunotherapies utilizing artificial intelligence to optimize patient selection and treatment protocols.

    Immunometabolic Interactions in Obesity: Implications for Therapeutic Strategies · 2025 · DOI

  • Although the exact underlying mechanisms remain unclear, it has been hypothesized that the adipose tissue dysfunction that occurs in obesity leads to systemic inflammation and to the alteration of the BBB resulting in neuroinflammation and cognitive decline.

    From Obesity to Mitochondrial Dysfunction in Peripheral Tissues and in the Central Nervous System · 2025 · DOI

  • Despite these advances, key questions remain unresolved. What signals initiate adipose inflammation? Which cell types respond first, and how is this response coordinated over time? How do adipocytes, APCs, immune cells, and stromal elements communicate to support adipose expansion, and when does this initially adaptive response become maladaptive and pathological?

    How Adipocytes Orchestrate Inflammation Within Adipose Tissue? · 2025 · DOI

  • Real-time quantitative PCR and droplet digital PCR for plant miRNAs in mammalian blood provide little evidence for general uptake of dietary miRNAs: Limited evidence for general uptake of dietary plant xenomiRs.

    Emerging Biomarkers and Nanobiosensing Strategies in Diabetes · 2025 · DOI

  • Several studies examined targeting FXR as a modality to treat obesity with varying conflicting results, emphasizing the need to study tissue-specific roles of FXR.

    Deleting adipose FXR exacerbates metabolic defects and induces endocannabinoid lipid, 2-oleoyl glycerol, in obesity · 2025 · DOI

  • The role of cyclooxygenase-2 (COX-2), a well-known pharmacological target for attenuating inflammation, in regulating obesity and its comorbidities remains unclear.

    Global deletion of COX-2 attenuates hepatic inflammation but impairs metabolic homeostasis in diet-induced obesity · 2025 · DOI

  • Significant progress has been made in the development of complement-targeted drugs, with several agents approved or currently in clinical trials, targeting different components of the complement system. C5 inhibitors such as eculizumab and ravulizumab are the most widely used, blocking C5 cleavage to inhibit terminal complement pathway activation and thereby reducing the formation of C5b-9.

    Complement–Metabolic Inflammation Crosstalk: Molecular Mechanisms and Therapeutic Targets in Type 2 Diabetes and Its Complications · 2026 · DOI

  • For example, the detection of clonal haematopoiesis of indeterminate significance has been leveraged to finetune risk stratification tailor therapeutic targets.

    The Interplay Between Immunity, Inflammation and Endothelial Dysfunction · 2025 · DOI

  • Investigate the therapeutic relevance of selective modulation of the adipocyte MKK3-p38β-p70S6K pathway for improving adipose insulin sensitivity, - Determine the molecular substrate linking p38β to mTORC1-S6K1 in adipocytes, - Examine how p38β restrains mTORC1-S6K1 signaling…

    An Adipocyte MKK3–p38β Axis Preserves Insulin Responsiveness in Mice and Is Reciprocally Altered in Human Obesity · 2026 · DOI

  • These findings underscore the importance of gender, physical fitness, and multiple cardiovascular risk factors in the relationship between BMI and CRP, providing new perspectives for further research into the potential application value of these risk indicators in CVD prevention.

    Gender-Specific Moderating Role of Physical Fitness and Cardiovascular Risk Factors in the Relationship Between BMI and C-Reactive Protein: Cross-Sectional Study · 2025 · DOI

Most-cited papers in Adipokines, Inflammation, and Metabolic Diseases

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Open questions raised by papers listed on this page include: (1) Most of the causal and mechanistic evidence, including that for EV-mediated, angiocrine, EndMT-related and lymphatic mechanisms, derives from mouse and in vitro models and remains to be validated in human adipose tissue (“Breakdown of adipocyte-endothelial communication as a driver of adipose tissue…”, 2026); (2) Several important questions arising from the present framework remain unresolved (“Prometheus’s Fire, Part I: The Flight of Icarus—Molecular Mechanisms Underlying…”, 2026); (3) The relationships between each CTRP and these receptors have not yet been fully elucidated (“The contribution of the CTRP family and its receptors to fibrotic diseases”, 2026); (4) The mechanisms and pathways by which elevated Gal-4 concentrations are associated with obesity, diabetes, and cardiovascular disease are not yet known (“Molecular Mechanisms Linking Obesity and Type 2 Diabetes: Pathogenesis,…”, 2026); (5) Most of the existing research has focused on individual inflammatory proteins, while the role of inflammatory protein signatures associated with IR and cognition remains unexplored (“Inflammatory protein signatures as predictors of insulin resistance and…”, 2026). 551 gap statements have been mined from Adipokines, Inflammation, and Metabolic Diseases papers in our 7.9M-paper local library, which holds 1,803 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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