Biomedical subjects

Patrick Schrauwen

Publications and source records attributed to Patrick Schrauwen.

At least 19 recordsLinked to original sources

PubMed2026

Acute mild cold exposure with shivering reduces 24 h glucose levels in individuals with type 2 diabetes but not prediabetes.

AIMS/HYPOTHESIS: Repeated cold exposure with shivering has been proposed as a potential strategy to enhance glucose metabolism by increasing energy expenditure and substrate utilisation. However, acute effects/benefits of cold-induced shivering on glucose homeostasis in metabolically compromised individuals are unknown. Here, we aimed to determine whether cold exposure at two different intensities improves 24 h glucose homeostasis in individuals with prediabetes and type 2 diabetes. METHODS: In a randomised crossover trial conducted in the South Limburg/Maastricht region of the Netherlands, men and postmenopausal women with prediabetes (n=12) and stable type 2 diabetes (n=12), aged 40-75 years, body mass index ≥27 and ≤35 kg/m2, non-smoking and sedentary, underwent two whole-body cold exposure sessions using a water-perfused suit. Session order was randomised using an online randomisation tool (randomizer.org); participants were masked to the cold exposure intensity received, but investigators were not. Sessions were designed to elicit ~1.5-fold (mild, 15°C) and ~2.5-fold (moderate, 4°C) increases in resting metabolic rate (RMR). Continuous glucose monitoring assessed interstitial glucose concentrations over 24 h periods before and after each intervention, with controlled diet and activity. Shivering was confirmed via indirect calorimetry and electromyography. RESULTS: In both study groups and periods, RMR increased significantly vs baseline (p<0.001 for all). In prediabetes, the increase in the final 1 h of cold was 1.53 × RMR in mild and 1.94 × RMR in moderate cold. In type 2 diabetes, the increase was 1.57 × RMR and 2.09 × RMR in the final 1 h of mild and moderate cold, respectively. In prediabetes, neither mild nor moderate cold exposure altered mean 24 h glucose levels. In contrast, after mild cold exposure the type 2 diabetes group exhibited a significant reduction in mean 24 h glucose levels (-0.6 ± 0.5 mmol/l, p=0.003) and fasting glucose (-0.6 ± 0.8 mmol/l, p=0.019), as well as an increase in time in normal range (+8.8 ± 10.3%, p=0.013) and reduced time in hyperglycaemia (-10.9 ± 12.9%, p=0.014). Moderate cold did not significantly affect any of the glucose outcomes in type 2 diabetes. Baseline fasting glucose, age and ALT levels were predictors of the glucose-lowering response, suggesting greater benefits in individuals who have higher baseline glucose levels, are younger and/or have more optimal liver health, i.e. lower ALT. CONCLUSIONS/INTERPRETATION: Acute mild cold exposure with shivering reduced 24 h glucose levels in individuals with type 2 diabetes. No changes were observed in prediabetes. The observed effects appear to depend on baseline metabolic status rather than acute substrate utilisation during cold exposure. These findings support the potential of cold exposure as an adjunct non-pharmacological therapy for type 2 diabetes, although further mechanistic studies and validation in larger cohorts are warranted. TRIAL REGISTRATION: ClinicalTrials.gov NCT05576025 FUNDING: Dutch Organisation for Knowledge and Innovation in Health, Healthcare and Well-being (ZonMw): 09120012010062.

Humans↗

PubMed2006

UCP3 in muscle wasting, a role in modulating lipotoxicity?

UCP3 has been postulated to function in the defense against lipid-induced oxidative muscle damage (lipotoxicity). We explored this hypothesis during cachexia in rats (zymosan-induced sepsis), a condition characterized by increased oxidative stress and supply of fatty acids to the muscle. Muscle UCP3 protein content was increased 2, 6 and 11 days after zymosan injection. Plasma FFA levels were increased at day 2, but dropped below control levels on days 6 and 11. Muscular levels of the lipid peroxidation byproduct 4-hydroxy-2-nonenal (4-HNE) were increased at days 6 and 11 in zymosan-treated rats, supporting a role for UCP3 in modulating lipotoxicity during cachexia.

Aldehydes↗

PubMed2006

Involvement of UCP3 in mild uncoupling and lipotoxicity.

Although vital to life, mitochondria are also the major source of ROS production, which may have unwanted detrimental effects on DNA, RNA and protein structures Therefore, mitochondria must exhibit well-developed mechanisms to regulate its ROS production. One such mechanism might be mild uncoupling of the mitochondrial respiratory chain, thereby lowering the proton gradient across the inner mitochondrial membrane and directly lowering ROS production. Mitochondrial uncoupling proteins have been shown to possess mild uncoupling activity and may therefore be important regulator of mitochondrial ROS production. The skeletal muscle isoform of the uncoupling protein family, UCP3, seems to be specifically active under conditions of high fatty acid availability. Although the exact function of UCP3 is not yet unravelled, UCP3 is activated by lipid peroxides and suggested to export fatty acid anions and/or peroxides from the mitochondrial matrix, thereby specifically protecting fatty acids from ROS-induced oxidative damage. Protein levels of UCP3 are reduced with aging and in the (pre)-diabetic state, both conditions characterized by increased levels of oxidative damage to lipids and proteins and reduced mitochondrial function. Whether UCP3 is causally related to mitochondrial dysfunction and is essential in the prevention and treatment of lipid-induced mitochondrial dysfunction requires further study.

Adenosine Triphosphate↗

PubMed2006

The effect of high-fat feeding on intramuscular lipid and lipid peroxidation levels in UCP3-ablated mice.

Uncoupling protein-3 (UCP3) has been suggested to protect against lipid-induced oxidative damage. Therefore, we studied intramuscular lipid peroxide levels and high-fat diet induced alterations in muscle lipid metabolism of UCP3-ablated mice. UCP3-/- mice showed approximately 3-fold higher levels of intramuscular lipid peroxides upon standard chow feeding, compared to wild-type littermates. Remarkably, this difference was no longer apparent on the high-fat diet. However, upon high-fat feeding, intramuscular triacylglycerol levels were approximately 50% lower in UCP3-/- mice, in comparison to UCP3+/+ animals. Succinate dehydrogenase activity, and total protein content of the muscle fatty acid transporter FAT/CD36 were however similar between UCP3-/- and UCP3+/+ mice.

Animals↗

PubMed2006

Regional variations in intramyocellular lipid concentration correlate with muscle fiber type distribution in rat tibialis anterior muscle.

1H MR spectroscopy (MRS) has proved to be a valuable noninvasive tool to measure intramyocellular lipids (IMCL) in research focused on insulin resistance and type II diabetes in both humans and rodents. An important determinant of IMCL is the muscle fiber type, since oxidative type I fibers can contain up to three times more IMCL than glycolytic type II muscle fibers. Because these different muscle fiber types are inhomogeneously distributed in rodent muscle, in the present study we investigated the distribution of IMCL within the rat tibialis anterior muscle (TA) in vivo using single-voxel 1H MRS along with the muscle fiber distribution in the TA ex vivo determined from immunohistological assays. IMCL levels in the TA differed by up to a factor of 3 depending on the position of the voxel. The distribution of IMCL over the TA cross section was not random, but emerged in a pattern similar to the distribution of the predominantly oxidative muscle fiber types. Dietary interventions, such as high-fat feeding and 15 hr of fasting, did not significantly change this typical fiber type-dependent pattern of IMCL content. These results stress the importance of voxel positioning when single-voxel 1H MRS is used to study IMCL in rodent muscle.

Animal Feed↗

PubMed2006

Intramyocellular lipid content in human skeletal muscle.

Fat can be stored not only in adipose tissue but also in other tissues such as skeletal muscle. Fat droplets accumulated in skeletal muscle [intramyocellular lipids (IMCLs)] can be quantified by different methods, all with advantages and drawbacks. Here, we briefly review IMCL quantification methods that use biopsy specimens (biochemical quantification, electron microscopy, and histochemistry) and non-invasive alternatives (magnetic resonance spectroscopy, magnetic resonance imaging, and computed tomography). Regarding the physiological role, it has been suggested that IMCL serves as an intracellular source of energy during exercise. Indeed, IMCL content decreases during prolonged submaximal exercise, and analogously to glycogen, IMCL content is increased in the trained state. In addition, IMCL content is highest in oxidative, type 1 muscle fibers. Together, this, indeed, suggests that the IMCL content is increased in the trained state to optimally match fat oxidative capacity and that it serves as readily available fuel. However, elevation of plasma fatty acid levels or dietary fat content also increases IMCL content, suggesting that skeletal muscle also stores fat simply if the availability of fatty acids is high. Under these conditions, the uptake into skeletal muscle may have negative consequences on insulin sensitivity. Besides the evaluation of the various methods to quantify IMCLs, this perspective describes IMCLs as valuable energy stores during prolonged exercise, which, however, in the absence of regular physical activity and with overconsumption of fat, can have detrimental effects on muscular insulin sensitivity.

Dietary Fats↗

PubMed2006

Eat the meat or feed the meat: protein turnover in remodeling muscle.

PURPOSE OF REVIEW: The present review outlines the role of muscle protein turnover in muscle remodeling, with emphasis on the effects of nutrition and exercise. RECENT FINDINGS: Progress in our understanding of the pathways signaling and regulating protein synthesis and degradation, and thus protein turnover, in skeletal muscle has been substantial over the past decade. Protein synthesis and degradation jointly allow the active remodeling of skeletal muscle to adapt to changes in mechanical and metabolic demand. Nutrition and exercise are potent ways to stimulate protein turnover. This occurs in an amino acid and exercise-type (resistance versus endurance) and mode (lengthening and shortening)-specific manner. SUMMARY: For optimal muscle remodeling, the timing and type of feeding and exercise appear to be crucial.

Dietary Proteins↗

PubMed2005

Reduced skeletal muscle uncoupling protein-3 content in prediabetic subjects and type 2 diabetic patients: restoration by rosiglitazone treatment.

CONTEXT: The mitochondrial uncoupling protein-3 (UCP3) has been implicated in the protection of the mitochondrial matrix against lipid-induced mitochondrial damage. Recent evidence points toward mitochondrial aberrations as a major contributor to the development of insulin resistance and diabetes, and UCP3 is reduced in diabetes. OBJECTIVE: We compared skeletal muscle UCP3 protein levels in prediabetic subjects [i.e. impaired glucose tolerance (IGT)], diabetic patients, and healthy controls and examined whether rosiglitazone treatment was able to restore UCP3. PATIENTS, DESIGN, INTERVENTION: Ten middle-aged obese men with type 2 diabetes mellitus [age, 61.4 +/- 3.1 yr; body mass index (BMI), 29.8 +/- 2.9 kg/m(2)], nine IGT subjects (age, 59.0 +/- 6.6 yr; BMI, 29.7 +/- 3.0 kg/m(2)), and 10 age- and BMI-matched healthy controls (age, 57.3 +/- 7.4 yr; BMI, 30.1 +/- 3.9 kg/m(2)) participated in this study. After baseline comparisons, diabetic patients received rosiglitazone (2 x 4 mg/d) for 8 wk. MAIN OUTCOME MEASURES: Muscle biopsies were sampled to determine UCP3 and mitochondrial protein (complex I-V) content. RESULTS: UCP3 protein content was significantly lower in prediabetic IGT subjects and in diabetic patients compared with healthy controls (39.0 +/- 28.5, 47.2 +/- 24.7, and 72.0 +/- 23.7 arbitrary units, respectively; P < 0.05), whereas the levels of the mitochondrial protein complex I-V were similar between groups. Rosiglitazone treatment for 8 wk significantly increased insulin sensitivity and muscle UCP3 content (from 53.2 +/- 29.9 to 66.3 +/- 30.9 arbitrary units; P < 0.05). CONCLUSION: We show that UCP3 protein content is reduced in prediabetic subjects and type 2 diabetic patients. Eight weeks of rosiglitazone treatment restores skeletal muscle UCP3 protein in diabetic patients.

Aged↗

PubMed2005

Exercise training restores uncoupling protein-3 content in limb muscles of patients with chronic obstructive pulmonary disease.

Oxidative capacity and uncoupling protein-3 (UCP3) content are reduced in limb muscles of patients with chronic obstructive pulmonary disease (COPD). It has been hypothesized that the physiological role of UCP3 is to protect mitochondria against lipotoxicity in cases where fatty acid influx exceeds the capacity to oxidize them. Exercise training improves oxidative capacity and reduces UCP3 protein content in healthy subjects, but the response of UCP3 to training in COPD is unknown. We studied the effect of exercise training on UCP3 content in limb muscles of COPD patients. For this, seven healthy age-matched subjects and thirteen patients with COPD were studied. All patients were admitted to an 8-wk exercise training intervention. Exercise capacity was assessed by means of an incremental cycle ergometry test. Biopsies were taken from the vastus lateralis in which UCP3 and lipid peroxidation levels were determined by Western blotting. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase (HAD; an enzyme involved in fatty acid oxidation) were measured as indexes of muscle oxidative capacity. UCP3 in COPD was approximately 50% lower compared with healthy age-matched controls. In COPD, training induced upregulation of UCP3 [from 67.7 (SD 41.8) to 113.8 (SD 104.2) arbitrary units (AU), P = 0.062], especially in the patients who showed no increase in HAD activity [from 80.9 (SD 52.6) to 167.9 (SD 109.1) AU, P = 0.028], whereas lipid peroxidation levels remained unaltered. We conclude that exercise-training can restore muscle UCP3 protein level in COPD, and the nature of this response complies with the hypothesis that UCP3 may protect against lipotoxicity.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2005

Putative function and physiological relevance of the mitochondrial uncoupling protein-3: involvement in fatty acid metabolism?

The discovery of the human homologue of the thermogenic protein UCP1, named uncoupling protein 3 (UCP3), boosted research on the role of this skeletal muscle protein in energy metabolism and body weight regulation. Nowadays, 9 years after its discovery emerging data indicate that the primary physiological role of UCP3 may be the mitochondrial handling of fatty acids rather than regulating energy expenditure via thermogenesis. UCP3 has been proposed to export fatty acid anions or fatty acid peroxides away from the matrix-side of the mitochondrial inner membrane to prevent their deleterious accumulation. In this way, UCP3 could protect mitochondria against lipid-induced oxidative mitochondrial damage, a function especially important under conditions of high fatty acid supply to skeletal muscle mitochondria. Such function may be clinically relevant in the development of type 2 diabetes mellitus, a condition characterized by muscular fat accumulation, mitochondrial damage and low levels of UCP3.

Animals↗

PubMed2005

Glucose ingestion during exercise blunts exercise-induced gene expression of skeletal muscle fat oxidative genes.

Ingestion of carbohydrate during exercise may blunt the stimulation of fat oxidative pathways by raising plasma insulin and glucose concentrations and lowering plasma free fatty acid (FFA) levels, thereby causing a marked shift in substrate oxidation. We investigated the effects of a single 2-h bout of moderate-intensity exercise on the expression of key genes involved in fat and carbohydrate metabolism with or without glucose ingestion in seven healthy untrained men (22.7 +/- 0.6 yr; body mass index: 23.8 +/- 1.0 kg/m(2); maximal O(2) consumption: 3.85 +/- 0.21 l/min). Plasma FFA concentration increased during exercise (P < 0.01) in the fasted state but remained unchanged after glucose ingestion, whereas fat oxidation (indirect calorimetry) was higher in the fasted state vs. glucose feeding (P < 0.05). Except for a significant decrease in the expression of pyruvate dehydrogenase kinase-4 (P < 0.05), glucose ingestion during exercise produced minimal effects on the expression of genes involved in carbohydrate utilization. However, glucose ingestion resulted in a decrease in the expression of genes involved in fatty acid transport and oxidation (CD36, carnitine palmitoyltransferase-1, uncoupling protein 3, and 5'-AMP-activated protein kinase-alpha(2); P < 0.05). In conclusion, glucose ingestion during exercise decreases the expression of genes involved in lipid metabolism rather than increasing genes involved in carbohydrate metabolism.

AMP-Activated Protein Kinases↗

PubMed2005

Regulation of metabolic transcriptional co-activators and transcription factors with acute exercise.

Endurance exercise improves insulin sensitivity and increases fat oxidation, which are partly facilitated by the induction of metabolic transcription factors. Next to exercise, increased levels of FFA's also increase the gene expression of transcription factors, hence making it difficult to discern the effects from contractile signals produced during exercise, from those produced by increased circulatory FFA's. We aimed to investigate, in human skeletal muscle, whether acute exercise affects gene expression of metabolic transcriptional co-activators and transcription factors, including PGC-1alpha, PRC, PPARalpha, beta/delta, and gamma and RXR, SREBP-1c and FKHR, and to discern the effect of exercise per se from those of elevated levels of FFA. Two hours of endurance exercise was performed either in the fasted state, or following carbohydrate ingestion prior to and during exercise, thereby blunting the fasting-induced increase in FA availability and oxidation. Of the genes measured, PGC-1alpha and PRC mRNA increased immediately after, while PPARbeta/delta and FKHR mRNA increased 1-4 h after exercise, irrespective of the increases in FFA's. Our results suggest that the induction in vivo of metabolic transcription factors implicated in mitochondrial biogenesis are under the control of inherent signals, (PGC-1alpha, PRC), while those implicated in substrate selection are under the control of associated signals (PPARbeta/delta, FKHR) stimulated from the contracting skeletal muscle that are independent of circulating FFA levels.

Dietary Carbohydrates↗

PubMed2005

Intramyocellular lipid content and molecular adaptations in response to a 1-week high-fat diet.

OBJECTIVE: To investigate molecular adaptations that accompany the elevation of intramyocellular lipid (IMCL) content on a high-fat (HF) diet for 1 week. RESEARCH METHODS AND PROCEDURES: Ten subjects consumed a normal-fat (NF) diet for 1 week, followed by an HF diet for another week. After both dietary periods, we determined the IMCL content by proton magnetic resonance spectroscopy in the vastus lateralis muscle and quantified changes in gene expression, protein content, and activity in biopsy samples. We investigated genes involved in carbohydrate and fatty acid handling [lipoprotein lipase, acetyl-coenzyme A carboxylase (ACC) 2, hormone-sensitive lipase, hexokinase II, and glucose transporter 4] and measured protein levels of CD36 and phosphorylated and unphosphorylated ACC2 and the activity of adenosine monophosphate-activated kinase. RESULTS: IMCL content was increased by 54% after the HF period. Lipoprotein lipase mRNA concentration was increased by 33%, whereas ACC2 mRNA concentration tended to be increased after the HF diet. Hexokinase II, glucose transporter 4, and hormone-sensitive lipase mRNA were unchanged after the HF diet. ACC2 and CD36 protein levels, phosphorylation status of ACC2, and adenosine monophosphate-activated kinase activity did not change in response to the HF diet. DISCUSSION: We found that IMCL content in skeletal muscle increased after 1 week of HF feeding, accompanied by molecular adaptations that favor fat storage in muscle rather than oxidation.

Acetyl-CoA Carboxylase↗

PubMed2005

Systemic inflammation correlates with increased expression of skeletal muscle ubiquitin but not uncoupling proteins in cancer cachexia.

Muscle wasting in experimental cancer cachexia has been associated with increased ubiquitin proteasome proteolytic system activity and increased uncoupling protein (UCP) expression. Increased ubiquitin proteasome pathway activity has also been found in gastric, but not lung, cancer patients. It therefore remains unclear in which patients modulation of this proteolytic system could be a therapeutic target. We investigated markers of systemic inflammation, hypermetabolism and expression of ubiquitin and uncoupling proteins 2 and 3 in muscle of pancreatic cancer patients. Rectus abdominis muscle was sampled from 15 weight-losing pancreatic cancer patients and 11 controls. UCP2 and 3, and ubiquitin mRNA expression were measured by Northern blots and UCP3 protein by Western blotting. Resting energy expenditure and plasma IL-6, sTNF-R and C-reactive protein (CRP) were also measured. Cancer patients had lost 18% of pre-illness stable weight, but were not significantly hypermetabolic compared with controls. IL-6, sTNF-R and CRP levels and ubiquitin 2.4 kb, but not 1.2 kb, mRNA expression were increased in cancer patients. UCP-2 and 3 mRNA and UCP-3 protein were similar in both groups. Weight loss correlated with systemic inflammation and ubiquitin 1.2 and 2.4 kb mRNA expression. Weight loss in pancreatic cancer is associated with systemic inflammation and increased mRNA expression for ubiquitin but not uncoupling proteins in skeletal muscle. The pro-inflammatory network and ubiquitin proteasome pathway may be targets for intervention in pancreatic cancer cachexia.

Aged↗

PubMed2004

DGAT1 overexpression in muscle by in vivo DNA electroporation increases intramyocellular lipid content.

In adipose tissue, the microsomal enzyme 1,2-acyl CoA:diacylglyceroltransferase-1 (DGAT1) plays an important role in triglyceride storage. Because DGAT1 is expressed in skeletal muscle as well, we aimed to directly test the effect of DGAT1 on muscular triglyceride storage by overexpressing DGAT1 using in vivo DNA electroporation. A pcDNA3.1-DGAT1 construct in saline was injected in the left tibialis anterior muscle of rats, followed by the application of eight transcutaneous pulses, using the contralateral leg as sham-electroporated control. Electroporation of the DGAT1 construct led to significant overexpression of the DGAT1 protein. The functionality of DGAT1 overexpression is underscored by the pronounced diet-responsive increase in intramyocellular lipid (IMCL) storage. In chow-fed rats, DGAT1-positive myocytes showed significantly higher IMCL content compared with the control leg, which was almost devoid of IMCL (1.99 +/- 1.13% vs. 0.017 +/- 0.014% of total area fraction; P <0.05). High-fat feeding increased IMCL levels in both DGAT1-positive and control myocytes, resulting in very high IMCL levels in DGAT1-overexpressing myocytes (4.96 +/- 1.47% vs. 0.80 +/- 0.14%; P <0.05). Our findings indicate that DGAT1 contributes to the storage of IMCL and that in vivo DNA electroporation is a promising tool to examine the functional consequences of altered gene expression in mature skeletal muscle.

Acyltransferases↗

PubMed2004

Intramyocellular lipids and insulin sensitivity: does size really matter?

Explore the source record for details and available documents.

Diglycerides↗

PubMed2004

The role of uncoupling protein 3 in fatty acid metabolism: protection against lipotoxicity?

The physiological function of the mitochondrial uncoupling protein (UCP), UCP3, is still under debate. There is, however, ample evidence to indicate that, in contrast to UCP1, the primary function of UCP3 is not the dissipation of energy. Rather, several lines of evidence suggest that UCP3 is associated with cellular fatty acid metabolism. The highest levels of expression of UCP3 have been found in type 2 glycolytic muscle fibres, and fasting and high-fat diets up regulate UCP3. This up-regulation is most pronounced in muscle with a low fat oxidative capacity. Acute exercise also up regulates UCP3, and this effect has been shown to be a result of the exercise-induced increase in plasma fatty acid levels. In contrast, regular physical activity, which increases fat oxidative capacity, reduces UCP3 content. Based on these data it has been postulated that UCP3 functions to export those fatty acids that cannot be oxidized from the mitochondrial matrix, in order to prevent fatty acid accumulation inside the matrix. Several experiments have been conducted to test this hypothesis. Blocking carnitine palmitoyltransferase 1, thereby reducing fat oxidative capacity, rapidly induces UCP3. High-fat diets, which increase the mitochondrial supply of fatty acids, also up regulate UCP. However, feeding a similar amount of medium-chain fatty acids, which can be oxidized inside the mitochondrial matrix and therefore does not need to be exported from the matrix, does not affect UCP3 protein levels. In addition, UCP3 is increased in patients with defective beta-oxidation and is reduced after restoring oxidative capacity. In conclusion, it is suggested that UCP3 has an important physiological function in facilitating outward transport from the mitochondrial matrix of fatty acid anions that cannot be oxidized, thereby protecting against lipid-induced mitochondrial damage.

Anions↗

PubMed2004

Oxidative capacity, lipotoxicity, and mitochondrial damage in type 2 diabetes.

Recent evidence points toward decreased oxidative capacity and mitochondrial aberrations as a major contributor to the development of insulin resistance and type 2 diabetes. In this article we will provide an integrative view on the interrelation between decreased oxidative capacity, lipotoxicity, and mitochondrial aberrations in type 2 diabetes. Type 2 diabetes is characterized by disturbances in fatty acid metabolism and is accompanied by accumulation of fatty acids in nonadipose tissues. In metabolically active tissues, such as skeletal muscle, fatty acids are prone to so-called oxidative damage. In addition to producing energy, mitochondria are also a major source of reactive oxygen species, which can lead to lipid peroxidation. In particular, the mitochondrial matrix, which contains DNA, RNA, and numerous enzymes necessary for substrate oxidation, is sensitive to peroxide-induced oxidative damage and needs to be protected against the formation and accumulation of lipids and lipid peroxides. Recent evidence reports that mitochondrial uncoupling is involved in the protection of the mitochondrial matrix against lipid-induced mitochondrial damage. Disturbances in this protection mechanism can contribute to the development of type 2 diabetes.

Carrier Proteins↗