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Context The precise glycemic impact and clinical relevance of postprandial exercise in type 1 diabetes (T1D) has not been clarified yet. Objective This work aimed to examine acute, subacute, and late effects of postprandial exercise on blood glucose (BG). Methods A randomized, controlled trial comprised 4 laboratory visits, with 24-hour follow-up at home. Participants included adults with T1D (n = 8), aged 44 ± 13 years, with body mass index of 24 ± 2.1. Intervention included 30 minutes of rest (CONTROL), walking (WALK), moderate-intensity (MOD), or intermittent high-intensity (IHE) exercise performed 60 minutes after a standardized meal. Main outcome measures included BG change during exercise/control (acute), and secondary outcomes included the subacute (≤2 h after) and late glycemic effects (≤24 h after). Results Exercise reduced postprandial glucose (PPG) excursion compared to CONTROL , with a consistent BG decline in all patients for all modalities (mean declines −45 ± 24, −71 ± 39, and −35 ± 21 mg/dL, during WALK , MOD , and IHE, respectively (P <.001). For this decline, clinical superiority was demonstrated separately for each exercise modality vs CONTROL. Noninferiority of WALK vs MOD was not demonstrated, noninferiority of WALK vs IHE was demonstrated, and equivalence of IHE vs MOD was not demonstrated. Hypoglycemia did not occur during exercise. BG increased in the hour after exercise (more than after CONTROL ; P <.001). More than half of participants showed hyperglycemia after exercise necessitating insulin correction. There were more nocturnal hypoglycemic events after exercise vs CONTROL (P <.05). Conclusion Postprandial exercise of all modalities is effective, safe, and feasible if necessary precautions are taken (ie, prandial insulin reductions), as exercise lowered maximal PPG excursion and caused a consistent and clinically relevant BG decline during exercise while there was no hypoglycemia during or shortly after exercise. However, there seem to be 2 remaining challenges: subacute postexercise hyperglycemia and nocturnal hypoglycemia. [ABSTRACT FROM AUTHOR]

Manipulation of circulating histidine-containing dipeptides (HCD) has been shown to affect the development of diabetes and early-stage diabetic nephropathy (DN). The aim of the present study was to investigate whether such interventions, which potentially alter levels of circulating HCD, also affect the development of advanced-stage DN. Two interventions, aerobic exercise training and overexpression of the human carnosinase-1 (hCN1) enzyme, were tested. BTBR ob/ob mice were either subjected to aerobic exercise training (20 wk) or genetically manipulated to overexpress hCN1, and different diabetes- and DN-related markers were compared with control ob/ob and healthy (wild-type) mice. An acute exercise study was performed to elucidate the effect of obesity, acute running, and hCN1 overexpression on plasma HCD levels. Chronic aerobic exercise training did not affect the development of diabetes or DN, but hCN1 overexpression accelerated hyperlipidemia and aggravated the development of albuminuria, mesangial matrix expansion, and glomerular hypertrophy of ob/ob mice. In line, plasma, kidney, and muscle HCD were markedly lower in ob/ob versus wild-type mice, and plasma and kidney HCD in particular were lower in ob/ob hCN1 versus ob/ob mice but were unaffected by aerobic exercise. In conclusion, advanced glomerular damage is accelerated in mice overexpressing the hCN1 enzyme but not protected by chronic exercise training. Interestingly, we showed, for the first time, that the development of DN is closely linked to renal HCD availability. Further research will have to elucidate whether the stimulation of renal HCD levels can be a therapeutic strategy to reduce the risk for developing DN. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to determine the impact of diabetic neuropathy (dNP) on the distal versus proximal comparison of weakness in lower and upper limb muscles of patients with type 2 Diabetes Mellitus (T2DM)., Methods: 19 healthy male controls without neuropathy (HC) and 35 male T2DM patients, without dNP (n=8), with sensory dNP (n=13) or with sensorimotor dNP (dNPsm; n=14), were enrolled in this study. Maximal isometric (IM) and isokinetic (IK) muscle strength and IK muscle endurance of the dominant knee, ankle and elbow, and maximal IM handgrip strength were measured by means of dynamometry., Results: Ankle muscle endurance was lower compared to the knee, independently of dNP (p<0.001). Maximal IK ankle muscle strength was also lower compared to the knee, albeit only in dNPsm (p=0.003). No differences were found between maximal IM handgrip and elbow strength., Conclusions: Our results suggest an impact of T2DM -with or without dNP- on lower limb muscle strength more distally than proximally, while this was not observed in the upper limb. The gradient of dNP seemed to be a determining factor for the maximal muscle strength, and not for muscle endurance, in the lower limb., Competing Interests: The authors have no conflict of interest.