“…This was in conformity to earlier studies, that demonstrated similarly high prevalence of asymptomatic CTS among patients with diabetes[12]. …”
Section: Discussionsupporting
confidence: 93%
“…Preclinical studies show that pioglitazone produces an increase in subcutaneous adipocyte surface and whole body adipocity[10,11]. Although mature visceral adipocytes have a greater propensity to proliferate than subcutaneous adipocytes, it is the latter that proliferates following pioglitazone treatment[12,13]. …”
AIMTo evaluate the impact of pioglitazone pharmacotherapy in median nerve electrophysiology in the carpal tunnel among type 2 diabetes patients.METHODSThe study was executed in patients with type 2 diabetes, treated with oral drugs, categorized under pioglitazone or non-pioglitazone group (14 in each group), and who received electrophysiological evaluation by nerve conduction velocity at baseline and 3 mo.RESULTSAt 3 mo, pioglitazone-category had inferior amplitude in sensory median nerve [8.5 interquartile range (IQR) = 6.5 to 11.5) vs non-pioglitazone 14.5 (IQR 10.5 to 18.75)] (P = 0.002). Non-pioglitazone category displayed amelioration in amplitude in the sensory median nerve [baseline 13 (IQR = 9 to 16.25) vs 3 mo 8.5 (IQR = 6.5 to 11.5)] (P = 0.01) and amplitude in motor median nerve [baseline 9 (IQR = 4.75 to 11) vs 3 mo 6.75 (IQR = 4.75 to 10.25)] (P = 0.049); and deterioration of terminal latency of in motor ulnar nerve [baseline 2.07 (IQR = 1.92 to 2.25) vs 3 mo 2.16 (IQR = 1.97 to 2.325)] (P = 0.043). There was amelioration of terminal latency in sensory ulnar nerve [baseline 2.45 (IQR = 2.315 to 2.88) vs 3 mo 2.37 (IQR = 2.275 to 2.445) for pioglitazone group (P = 0.038).CONCLUSIONTreatment with pioglitazone accentuates probability of compressive neuropathy. In spite of comparable glycemic control over 3 mo, patients treated with pioglitazone showed superior electrophysiological parameters for the ulnar nerve. Pioglitazone has favourable outcome in nerve electrophysiology which was repealed when the nerve was subjected to compressive neuropathy.
“…This was in conformity to earlier studies, that demonstrated similarly high prevalence of asymptomatic CTS among patients with diabetes[12]. …”
Section: Discussionsupporting
confidence: 93%
“…Preclinical studies show that pioglitazone produces an increase in subcutaneous adipocyte surface and whole body adipocity[10,11]. Although mature visceral adipocytes have a greater propensity to proliferate than subcutaneous adipocytes, it is the latter that proliferates following pioglitazone treatment[12,13]. …”
AIMTo evaluate the impact of pioglitazone pharmacotherapy in median nerve electrophysiology in the carpal tunnel among type 2 diabetes patients.METHODSThe study was executed in patients with type 2 diabetes, treated with oral drugs, categorized under pioglitazone or non-pioglitazone group (14 in each group), and who received electrophysiological evaluation by nerve conduction velocity at baseline and 3 mo.RESULTSAt 3 mo, pioglitazone-category had inferior amplitude in sensory median nerve [8.5 interquartile range (IQR) = 6.5 to 11.5) vs non-pioglitazone 14.5 (IQR 10.5 to 18.75)] (P = 0.002). Non-pioglitazone category displayed amelioration in amplitude in the sensory median nerve [baseline 13 (IQR = 9 to 16.25) vs 3 mo 8.5 (IQR = 6.5 to 11.5)] (P = 0.01) and amplitude in motor median nerve [baseline 9 (IQR = 4.75 to 11) vs 3 mo 6.75 (IQR = 4.75 to 10.25)] (P = 0.049); and deterioration of terminal latency of in motor ulnar nerve [baseline 2.07 (IQR = 1.92 to 2.25) vs 3 mo 2.16 (IQR = 1.97 to 2.325)] (P = 0.043). There was amelioration of terminal latency in sensory ulnar nerve [baseline 2.45 (IQR = 2.315 to 2.88) vs 3 mo 2.37 (IQR = 2.275 to 2.445) for pioglitazone group (P = 0.038).CONCLUSIONTreatment with pioglitazone accentuates probability of compressive neuropathy. In spite of comparable glycemic control over 3 mo, patients treated with pioglitazone showed superior electrophysiological parameters for the ulnar nerve. Pioglitazone has favourable outcome in nerve electrophysiology which was repealed when the nerve was subjected to compressive neuropathy.
“…Furthermore, the primary function of PGZ is to increase the IMF deposition, and improvement of the meat flavor and taste has already been proven in pigs . Intensive research has ascribed the mechanism to the role of PGZ as an affinity ligand of PPAR γ , promoting adipocyte proliferation and fat accumulation . Undoubtedly, we found that supplementation with 7.5 mg kg −1 PGZ and 15 mg kg −1 PGZ increased the IMF by 14.14% and 20.37%, respectively.…”
Section: Discussionmentioning
confidence: 64%
“…28 Intensive research has ascribed the mechanism to the role of PGZ as an affinity ligand of PPAR , promoting adipocyte proliferation and fat accumulation. 29,30 Undoubtedly, we found that supplementation with 7.5 mg kg −1 PGZ and 15 mg kg −1 PGZ increased the IMF by 14.14% and 20.37%, respectively. In this regard, the drip loss, cooking loss, and shear force displayed a negative correlation but positive effects with 15 mg kg −1 PGZ supplementation.…”
“…Moreover, primary cultured adipocytes using ceiling culture showed an increase in cell number and incorporated BrdU. We have found that BrdU is incorporated more actively in small adipocytes (<20 µm in diameter) than large ones [12] in histological examination. However, it was hard to discriminate these cells from non-adipocytes.…”
Section: Growth Of Adipose Tissue In Leto and Oletf Ratsmentioning
Obesity consists of hypertrophy and hyperplasia of adipocytes. Although the number of adipocytes is influenced by anatomical location, nutritional environment, hormone and genetic variation, it has been thought to be determined by the proliferation of precursor cells and subsequent differentiation. However, our recent research has identified the population of small adipocytes less than 20 μm in diameter, exhibiting tiny or no lipid droplets and expressing adipocyte marker proteins (small proliferative adipocytes: SPA) in isolated adipocytes. Notably, 5-bromo-2'-deoxyuridine (BrdU) incorporation and proliferating cell nuclear antigen (PCNA) expression were detected in these cells. In this study, we investigated the role of SPA in development of adipose tissue using genetically obese diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats and their non-obese and non-diabetic littermates, Long-Evans Tokushima Otsuka (LETO) rats. Proliferation of SPA was determined by measurement of PCNA at the protein level in isolated fractions of adipocytes with collagenase digestion. In general, expression levels of PCNA rose, reached a maximum, and declined in adipose tissues during aging. The expression levels of PCNA were maximum in epididymal fat at 32 w and 12 w of age in LETO and OLETF, respectively. They reached the maximum at 20 w of age both in LETO and OLETF in mesenteric fat. Although the PCNA expression level was higher in OLETF in the early period, it reversed later. Enlargement of adipocytes developed during aging, which was enhanced when the expression levels of PCNA declined. These results suggest that proliferation of SPA may prevent adipocyte hypertrophy and the resultant development of metabolic disorders.
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