Pongpan Tanajak

ORCID: 0000-0003-1656-0574
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Research Areas
  • Fibroblast Growth Factor Research
  • Diabetes Treatment and Management
  • Metabolism, Diabetes, and Cancer
  • Pancreatic function and diabetes
  • Kruppel-like factors research
  • Epigenetics and DNA Methylation
  • Cardiovascular Function and Risk Factors
  • Salivary Gland Disorders and Functions
  • Heart Rate Variability and Autonomic Control
  • Diet and metabolism studies
  • Neuropeptides and Animal Physiology
  • Vagus Nerve Stimulation Research
  • Regulation of Appetite and Obesity
  • Effects of Radiation Exposure
  • Biochemical effects in animals
  • Mitochondrial Function and Pathology
  • Lung Cancer Research Studies
  • Peripheral Nerve Disorders
  • Cardiac Arrest and Resuscitation
  • Metabolomics and Mass Spectrometry Studies
  • Adipose Tissue and Metabolism
  • Stress Responses and Cortisol
  • Dietary Effects on Health
  • Shoulder Injury and Treatment
  • Nerve Injury and Rehabilitation

Chiang Mai University
2015-2018

Sodium-glucose cotransporter 2 inhibitor (SGLT2-i) effects on cardiac ischemia/reperfusion (I/R) injury are unclear. Unlike SGLT2-i, dipeptidyl peptidase 4 inhibitors (DPP4-i) have shown effective cardioprotection in I/R injury. We aimed to investigate whether SGLT2-i reduces myocardial dysfunction and a greater extent than DPP4-i obese insulin-resistant rats with/without The high-fat (HF) diet-induced were divided into groups received the following treatments for 28 days: vehicle (HFV);...

10.1530/joe-17-0457 article EN Journal of Endocrinology 2017-11-16

Abstract Dipeptidyl peptidase-4 (DDP-4) inhibitors and energy restriction (ER) are widely used to treat insulin resistance type 2 diabetes mellitus. However, the effects of ER or combination with vildagliptin on brain sensitivity, mitochondrial function, hippocampal synaptic plasticity cognitive function in obese insulin-resistant rats have never been investigated. We hypothesised that DDP-4 inhibitor exerts better efficacy than alone improving cognition male by restoring plasticity. A total...

10.1017/s0007114516003871 article EN British Journal Of Nutrition 2016-11-17

Propose: To investigate the temporal relationship between plasma fibroblast growth factor 21 levels, insulin resistance, metabolic dysfunction and cardiac resistance in long-term high-fat diet-induced obese rats.In total, 36 male Wistar rats were fed with either a normal diet or for 12 weeks. Blood was collected from tail tip, used to determine profiles levels. Rats sacrificed at weeks 4, 8 12, hearts rapidly removed determination of signalling pathways.Body weight levels increased after 4...

10.1177/1479164118757152 article EN Diabetes and Vascular Disease Research 2018-02-09

Abstract Estrogen deprivation aggravates cardiac injury after myocardial ischemia and reperfusion (I/R) injury. Although either estrogen or the dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, reduces damage following I/R, their effects on heart in obese-insulin resistant deprived conditions remain unknown. Ovariectomized (O) rats (n = 36) were divided to receive normal diet (NDO) high-fat (HFO) for 12 weeks, followed by treatment with a vehicle, vildagliptin 4 weeks. The setting of...

10.1038/srep44306 article EN cc-by Scientific Reports 2017-03-10

Long-term high-fat diet (HFD) consumption causes cardiac dysfunction. Although calorie restriction (CR) has been shown to be useful in obesity, we hypothesized that combined CR with dipeptidyl peptidase-4 (DPP-4) inhibitor provides greater efficacy than monotherapy attenuating dysfunction and metabolic impairment HFD-induced obese-insulin resistant rats. Thirty male Wistar rats were divided into 2 groups fed on either a normal (ND, n = 6) or HFD ( 24) for 12 weeks. Then, 4 subgroups...

10.1530/joe-16-0406 article EN Journal of Endocrinology 2016-11-15

Long-term consumption of a high-fat diet (HFD) causes not only obese-insulin resistance, but is also associated with mitochondrial dysfunction in several organs. However, the effect resistance on salivary glands has been investigated. We hypothesized that induced by HFD impaired gland function reducing salivation, increasing inflammation, and fibrosis, as well impairing calcium transient signaling. Male Wistar rats (200-220 g) were fed either ND or an (n = 8/group) for 16 weeks. At end week...

10.1139/apnm-2016-0545 article EN Applied Physiology Nutrition and Metabolism 2016-12-21

Summary Aims Comparative efficacy between fibroblast growth factor 21 (FGF21) and vildagliptin on metabolic regulation, cardiac mitochondrial function, heart rate variability (HRV), left ventricular (LV) function is not known. We hypothesized that FGF21 share a similar in improving these parameters high fat diet (HFD)‐induced obese‐insulin resistant rats. Methods Twenty‐four male Wistar rats were fed with either normal (ND) or HFD for 12 weeks. Then, ND received vehicle (NDV). Rats the group...

10.1111/1755-5922.12263 article EN Cardiovascular Therapeutics 2017-04-09

The intricate interplay between cardiovascular health and metabolic regulation forms a critical junction in understanding the complexities of heart-related conditions. Cardiometabolic orchestrates sophisticated network factors governing energy utilization, substrate metabolism, cellular processes within system. Balancing these mechanisms is pivotal for optimal heart function, considering substantial demands both contractile non-contractile activities. In healthy heart, fatty acids (FAs)...

10.36922/itps.2302 article EN cc-by-nc INNOSC Theranostics and Pharmacological Sciences 2024-04-03

Breast cancer is a leading cause of mortality among women worldwide, necessitating surgical interventions like lumpectomy, mastectomy, or modified radical mastectomy. However, these procedures often lead to postoperative complications, such as frozen shoulder, significantly impacting patients’s quality life. This review focuses on the challenges associated with shoulder and other complications following breast surgery. It proposes integration Artificial Intelligence (AI) in assessment...

10.26420/chronicdisint.2023.1030 article EN Chronic Diseases - International 2023-11-08
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