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Found 12 results for "diabetes mellitus type"
Studies show that synthetic, genetically modified insulin could be to blame for a number of
GMI Research Group
18 min
Type 3 Diabetes is when the brain stops or reduces the acceptance of the brain
drgrantwellness
8 min
golden hue, in delaying the development of type 2 diabetes mellitus (T2DM) in a prediabetic population.
Sayer Ji
3 min
Originally published on www.orthomolecular.org by Max Langen More than 460 million people, almost 6% of the world's population, are suffering from type 2 diabetes, the most common form. Over 1 milli...
OrthomolecularNewsService
13 min
The title of this article may sound like heresy to those who have been schooled
Sayer Ji
11 min<p>OBJECTIVE: To observe the effect of electroacupuncture (EA) on the glucagon-like peptide-1 receptor (GLP-1R)/protein kinase A (PKA) signaling pathway in the colon tissue of type 2 diabetes mellitus (T2DM) rats and explore the mechanisms underlying EA's improvement of insulin resistance and intestinal mucosal barrier injury. METHODS: Among 24 SPF-grade male Wistar rats, 6 rats were randomly assigned to a blank group, and the remaining 18 rats were used to establish the T2DM model through a combination of high-sucrose/high-fat diet feeding and intraperitoneal injection of streptozotocin. Successfully modeled rats were randomly assigned to a model group, an EA group, and an EA+inhibitor group, with 6 rats per group. The EA group received EA at bilateral "Tianshu" (ST25), "Shangjuxu" (ST37), "Pishu" (BL20), and "Weiwanxiashu" (EX-B3); EA was applied to ipsilateral "Shangjuxu" (ST37) and "Weiwanxiashu" (EX-B3) using disperse-dense wave (2 Hz/50 Hz, 1-3 mA) for 20 min per session. The EA+inhibitor group received the same EA treatment combined with intraperitoneal injection of the GLP-1 receptor inhibitor Exenatide. All treatments were administered once daily, six times per week, for 6 weeks. Fasting blood glucose (FBG) was measured before modeling and before/after intervention. After the intervention, serum fasting insulin (FINS) and GLP-1 levels were measured by ELISA, and the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Colon morphology was observed using HE staining. Positive expression of zonula occludens-1 (ZO-1) and Occludin in colon tissue was detected by immunohistochemistry. Protein expression of GLP-1R, PKA, GLP-1, ZO-1, and Occludin in colon tissue was analyzed by Western blot. RESULTS: After the intervention, compared with the blank group, the model group showed significantly increased FBG, FINS, and HOMA-IR (P<0.01), while serum GLP-1 level was significantly decreased (P<0.01); histologically, the colonic mucosal epithelial cells exhibited shedding, crypt atrophy was observed, the number of goblet cells was markedly reduced, and inflammatory cell infiltration was evident in the lamina propria; the positive expression of ZO-1 and Occludin in colon tissue was significantly reduced (P<0.01, P<0.05), and the protein expression of GLP-1R, PKA, GLP-1, ZO-1, and Occludin was also significantly decreased (P<0.05, P<0.01). Compared with the model group and the EA+inhibitor group, the EA group showed significantly lower levels of FBG, FINS, and HOMA-IR (P<0.01), along with higher serum GLP-1 level (P<0.01); the inflammatory cell infiltration in the colon was reduced, the number of goblet cells was increased, and the structure of the mucosal epithelium and crypts was more normalized; the positive expression of ZO-1 and Occludin in colon tissue was significantly increased (P<0.01, P<0.05), and the protein expression of GLP-1R, PKA, GLP-1, ZO-1, and Occludin was also significantly elevated (P<0.05, P<0.01). CONCLUSION: EA could reduce blood glucose levels, improve insulin resistance, and repair intestinal mucosal barrier injury in T2DM rats. The underlying mechanism may be related to the activation of the GLP-1R/PKA signaling pathway. 目的：观察电针对2型糖尿病（T2DM）大鼠结肠胰高血糖素样肽-1受体（GLP-1R）/蛋白激酶A（PKA）信号通路的影响，探讨电针改善T2DM胰岛素抵抗及肠黏膜屏障损伤的相关机制。 方法：24只SPF级雄性Wistar大鼠中，随机选取6只作为空白组，剩余18只采用高糖高脂饲料喂养联合链脲佐菌素腹腔注射制备T2DM大鼠模型，将造模成功的大鼠随机分为模型组、电针组与电针+抑制剂组，每组6只。电针组予电针干预，穴取双侧“天枢”“上巨虚”“脾俞”“胃脘下俞”，同侧“上巨虚”“胃脘下俞”连接电针仪，选择疏密波，频率2 Hz/50 Hz，电流1~3 mA，每次20 min。电针+抑制剂组予电针联合腹腔注射GLP-1R抑制剂艾塞那肽，电针干预同电针组。均每日1次，每周6次，干预6周。检测各组大鼠造模前及干预前后空腹血糖（FBG）。干预后，采用ELISA法检测大鼠血清空腹胰岛素（FINS）及胰高血糖素样肽-1（GLP-1）含量，并计算胰岛素抵抗指数（HOMA-IR）；HE染色法观察大鼠结肠组织形态；免疫组化法检测大鼠结肠闭锁小带蛋白-1（ZO-1）、闭锁蛋白（Occludin）阳性表达；Western blot法检测大鼠结肠GLP-1R、PKA、GLP-1、ZO-1、Occludin蛋白表达。 结果：干预后，与空白组比较，模型组大鼠FBG、血清FINS含量、HOMA-IR升高（P<0.01），血清GLP-1含量降低（P<0.01），结肠黏膜上皮细胞脱落，隐窝萎缩，杯状细胞数量明显减少，固有层可见炎性细胞浸润，结肠ZO-1、Occludin阳性表达降低 （P<0.01，P<0.05），结肠GLP-1R、PKA、GLP-1、ZO-1、Occludin蛋白表达降低（P<0.05，P<0.01）；与模型组和电针+抑制剂组比较，电针组大鼠FBG、血清FINS含量、HOMA-IR降低（P<0.01），血清GLP-1含量升高 （P<0.01），结肠炎性细胞浸润减轻，杯状细胞数量及黏膜上皮、隐窝结构趋于正常，结肠ZO-1、Occludin阳性表达升高（P<0.01，P<0.05），结肠GLP-1R、PKA、GLP-1、ZO-1、Occludin蛋白表达升高（P<0.05，P<0.01）。 结论：电针可以降低T2DM大鼠血糖水平，改善胰岛素抵抗，修复肠黏膜屏障损伤，其机制可能与激活GLP-1R/PKA信号通路有关。.</p>
OBJECTIVE: The study examined the association between adiponectin levels and markers of Insulin Resistance (IR) in obese and non-obese adults with type 2 diabetes. Insulin Resistance was estimated using HOMA-IR, while group differences were assessed using appropriate statistical tests. Multiple linear regression was applied to evaluate associations between adiponectin and obesity indices while adjusting for HOMA-IR. RESULTS: Mean serum adiponectin did not differ significantly across obese diabetics, non-obese diabetics, and controls (5.9 ± 3.6 µg/mL, 6.4 ± 3.2 µg/mL, and 6.8 ± 3.5 µg/mL, respectively; p = 0.13). Mean HOMA-IR values were comparable among obese diabetics (1.4 ± 2.1), non-obese diabetics (1.3 ± 1.0), and controls (1.1 ± 0.6). In multivariable regression models, serum adiponectin was not independently associated with obesity indices or HOMA-IR (all p > 0.05). Serum adiponectin levels were not significantly different across the study groups, although numerically lower values were observed in obese individuals with diabetes. No significant relationship was found between adiponectin and clinical or biochemical markers of IR. These findings suggest that adiponectin may have limited utility as an isolated marker of IR in Nigerian adults with type 2 diabetes and underscore the need for larger, longitudinal studies to clarify its role.
OBJECTIVES: This study investigated the relationship between serum metabolomic profiles and diabetic kidney disease (DKD) risk in patients with type 2 diabetes mellitus (T2DM) stratified into three KDIGO-defined risk categories. METHODS: Serum samples from 48 patients were analyzed using untargeted liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-QTOF/MS). Participants were classified into low (n = 16), moderate (n = 16), and high (n = 16) DKD risk groups according to KDIGO guidelines. Differential metabolites were identified based on p-value, log fold change, and variable importance in projection (VIP), and subsequently subjected to pathway enrichment analysis. RESULTS: Comparative analysis revealed five differential metabolites between low- and moderate-risk groups, three between moderate- and high-risk groups, and three between low- and high-risk groups. Notably, sphinganine, arachidonic acid, and ornithine were progressively downregulated, whereas AFMK, L-arginine, lactosylceramide (LacCer), and lysophosphatidylcholine (lysoPC) were upregulated with increasing DKD risk. These metabolites mapped to disturbed pathways, including arginine and proline metabolism, sphingolipid metabolism, glycerophospholipid metabolism, arachidonic acid metabolism, and tryptophan metabolism. CONCLUSION: This study highlights progressive alterations in amino acid, lipid, and inflammatory pathways across DKD risk categories, suggesting that these stage-specific metabolomic signatures may serve as putative biomarkers for detection and monitoring of DKD progression in T2DM.
BACKGROUND: Obesity is common in type 2 diabetes mellitus (T2DM) and is associated with lower fracture risk. However, older adults with T2DM have higher fracture rates, suggesting distinct effects of T2DM on musculoskeletal health. We aimed to compare associations between components of T2DM and musculoskeletal health in community-dwelling older adults with obesity, with and without T2DM. METHODS: This cross-sectional study included adults aged ≥60 years with self-reported obesity (body mass index [BMI] ≥30 kg/m). Physical function was assessed by short physical performance battery (SPPB), handgrip strength, stair-climb and jumping mechanography. Dual-energy X-ray absorptiometry (DXA) measured body composition and areal BMD (aBMD). High-resolution peripheral quantitative computed tomography (HR-pQCT) assessed tibial bone densitometry and microarchitecture. RESULTS: Among 116 participants, 40 (34 %) had T2DM with a higher proportion of females (80 %) compared to those without T2DM (63 %). T2DM participants had higher glucose (31 % mmol/L, p < 0.0001), HbA1c (15 %, p < 0.0001) and HOMA-IR (136 %, p < 0.0001), and exhibited lower hand grip strength (11 % ± 10 %, p = 0.036), SPPB scores (5 % ± 2 %, p = 0.044), stair-climb power (5 % ± 2 % W/kg, p = 0.010) and vertical jump power (2 % ± 8 % W/kg, p = 0.038) compared to counterparts. There were no differences between groups for bone outcomes except increased total hip aBMD (10 % ± 0.2 % g/cm, p = 0.026) and trabecular thickness (5 % ± 0.03 % mm, p = 0.017). In all participants, total fat mass was associated with impaired physical function, while appendicular lean mass was positively associated with muscle power but negatively associated with cortical BMD. CONCLUSION: Older adults with obesity and T2DM demonstrate impaired muscle function and power, but have similar bone health and body composition, compared with those with obesity alone.
Complex diseases arise from the interplay of genetic and environmental factors. We present a case where complex diseases seem to coexist. A 12-month-old girl was referred for short stature and hypotonia. Initial evaluation revealed central hypothyroidism, growth hormone deficiency and a small pituitary gland with ectopic neurohypophysis. Replacement therapy improved growth, but developmental delay and strabismus ensued. At age 10, she experienced a first seizure treated with levetiracetam. At age 12, she presented diabetic ketoacidosis and functional insulin therapy was started; positive autoantibodies confirmed autoimmune etiology. Initial genetic testing performed by microarray analysis retrieved normal results, but exome sequencing revealed a heterozygous pathogenic variant in KANSL1 gene, allowing for the diagnosis of Koolen-de Vries syndrome. In this patient, Koolen-de Vries syndrome presented initially as hypopituitarism and only later epilepsy. Afterwards, type 1 diabetes mellitus ensued, highlighting the complexity of intertwined conditions.
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