Biomedical subjects

Achim Peters

Publications and source records attributed to Achim Peters.

23 records · Page 2Linked to original sources

PubMed2003

Modulation of hunger by plasma glucose and metformin.

The plasma glucose concentration is a major short-term regulator of hunger and food intake. In patients with diabetes, therapies lowering plasma glucose are frequently associated with body weight gain, suggesting that lowered plasma glucose leads to increased feelings of hunger and food intake. However, as many physiological and symptomatic responses to low plasma glucose are attenuated after repeated episodes of hypoglycemia, this may also pertain to feelings of hunger. Here we tested whether the stimulatory effect of low plasma glucose on feelings of hunger is likewise reduced by repeated episodes of hypoglycemia. As metformin has been shown to reduce plasma glucose levels without increasing body weight and also to decrease food intake, we tested for possible interacting effects of this substance with hypoglycemia-induced hunger. Feelings of hunger were assessed by rating scales during 3 consecutive hypoglycemic clamps performed on 2 consecutive d in 15 normal weight men. Subjects were tested once while being treated with 850 mg metformin twice daily and once while receiving placebo. Treatment was started 14 d before the clamp experiments and was performed in a random order and double-blind fashion. Hypoglycemia markedly enhanced feelings of hunger (P < 0.001). However, rated feelings of hunger on the first and last hypoglycemic clamps were comparable (P = 0.304). Compared with placebo, metformin decreased feelings of hunger during hypoglycemia (P = 0.015). This reduction was not associated with a decrease in posthypoglycemic food intake as measured by the number of cookies consumed after the last clamp (P = 0.676). Data indicate that the stimulatory effect of low plasma glucose on hunger is not attenuated after repeated episodes of hypoglycemia, which implies that, in contrast to other symptoms, hunger is not subject to adaptive attenuation upon repeated hypoglycemia. Metformin attenuates hypoglycemia-induced hunger, but does not appear to influence posthypoglycemic food intake.

Adult↗

PubMed2002

All-solid-state tunable continuous-wave ultraviolet source with high spectral purity and frequency stability.

We present a novel approach for the generation of higly frequency-stable, widely tunable, single-frequency cw UV light that is suitable for high-resolution spectroscopy. Sum-frequency generation (SFG) of two solid-state sources with a single cavity resonant for both fundamental waves is employed. Using a highly stable, narrow-linewidth frequency-doubled cw Nd:YAG laser as a master laser and slaving to it the SFG cavity and the other fundamental wave from a Ti:sapphire laser, we generate UV radiation of 33-mW output power around 313 nm. Alternatively, we use a diode laser instead of the Ti:sapphire laser and produce an output power of 2.1 mW at 313 nm. With both setups we obtain a continuous tunability of >15 GHz, short-term frequency fluctuations in the submegahertz range, a long-term frequency drift below 100 MHz/h, and stable operation for several hours. The theory of optimized doubly resonant SFG is also given.

Journal Article↗

PubMed2002

Short-term treatment with metformin decreases serum leptin concentration without affecting body weight and body fat content in normal-weight healthy men.

A weight-reducing effect of metformin has been demonstrated in obese subjects with and without diabetes. The mechanisms of this action are unclear, which may be partly due to the fact that in obese and diabetic patients the substance's effects result from a complex interaction with the distinct endocrine and metabolic disturbances in these patients. To dissociate primary from secondary action of metformin, we examined effects of the substance in normal-weight healthy subjects. Fifteen normal-weight men were treated with metformin (850 mg twice daily) or placebo for a 15-day period in a double-blind, placebo-controlled, cross-over study. Anthropometric, psychologic, cardiovascular, endocrine, and metabolic parameters were assessed before and at the end of the treatment period. Metformin did not affect body weight (P =.838) and body fat mass (P =.916). Yet, serum leptin concentration was distinctly reduced after metformin (P <.001). Also, metformin reduced the concentration of plasma glucose (P =.011), serum insulin (P=.044), and serum insulin-like growth factor -1 (IGF-1) (P=.013), while it increased serum glucagon concentration (P <.001). There were no effects of metformin on feelings of hunger, blood pressure, heart rate, resting energy expenditure, the respiratory quotient, free fatty acids, beta-hydroxybutyrate, glycerol, triglycerides, cholesterol, and uric acid (all P >.1). Data indicate that metformin decreases the serum leptin concentration even without affecting body weight and body composition in normal-weight men.

Adipose Tissue↗

PubMed2002

Acute and prolonged effects of insulin-induced hypoglycemia on the pituitary-thyroid axis in humans.

Secretory activity of the pituitary-thyroid axis and thyroid hormone metabolism show characteristic changes in response to different stressors often referred to as the euthyroid sick syndrome. Hypoglycemia is an acute metabolic stressor inducing various neuroendocrine responses, the effects of which on pituitary-thyroid secretory activity so far have been entirely neglected. We performed stepwise hypoglycemic and euglycemic clamps each lasting 6 hours in 30 healthy men. To assess the potential influence of hyperinsulinemia on pituitary-thyroid hormone release, 2 different rates of insulin infusion were used for the clamps. During the hypoglycemic clamps, serum thyroid-stimulating hormone (TSH) concentration decreased in comparison to the euglycemic condition on average by 28% +/- 4% (P <.001), while serum concentration of free triiodothyronine (fT3), free thyroxine (fT4), and thyroxine-binding globulin (TBG) remained unchanged. The effect did not depend on the rate of insulin infusion. To assess the prolonged effect of acute hypoglycemia on pituitary-thyroid secretory activity, serum TSH and thyroid hormone concentrations were subsequently measured in another 15 healthy men before and 18 hours after 2 consecutive hypoglycemic clamps together lasting about 270 minutes. Compared with values before the hypoglycemic clamps, serum levels of TSH, fT3, and fT4 were found to be still reduced (by 44% +/- 6%, 12% +/- 2%, and 10% +/- 1%, respectively) 18 hours after the last hypoglycemic episode (P <.001 for all comparisons). The observed hormonal changes after hypoglycemia were not accompanied by any change in resting energy expenditure (REE). Data indicate acute as well as prolonged inhibitory influences of hypoglycemia on pituitary-thyroid secretory activity. The pattern of changes suggests that hypoglycemia exerts its influence primarily at a central, ie, pituitary and/or hypothalamic, site of the axis.

Adult↗

PubMed2002

Vascular endothelial growth factor: a novel endocrine defensive response to hypoglycemia.

Glucose, the most important fuel for the brain, is supplied by the actions of counterregulatory hormones and the sympathetic nervous system. Yet to obtain access to the brain, glucose must pass the blood-brain barrier. Here we show that vascular endothelial growth factor (VEGF), a potent regulator of blood vessel function, is a candidate hormone for facilitating glucose passage across the blood-brain barrier under critical conditions. In 16 healthy men, VEGF serum concentrations increased under 6 h of insulin-induced hypoglycemic conditions from 86.1 +/- 13.4 to 211.6 +/- 40.8 pg/ml (P = 0.002), whereas in the hyperinsulinemic euglycemic control condition, no change was observed. During hypoglycemia serum VEGF, but no other counterregulatory hormone, was associated with preserved neurocognitive function, as measured with a memory test (r = 0.539; P = 0.031) and the Stroop interference task (r = 0.569; P = 0.021). Findings show that acute hypoglycemia is accompanied by a brisk increase in circulating VEGF concentration and that VEGF could mediate rapid adaptation of the brain to neuroglycopenia.

Adult↗