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Biomedical subjects

Michael Horowitz

Publications and source records attributed to Michael Horowitz.

At least 73 records · Page 4Linked to original sources
PubMed2004

Upper gastrointestinal responses to intraduodenal nutrient in type 1 diabetes mellitus.

BACKGROUND: Abnormal nutrient-related small-intestinal feedback may contribute to disordered gastric motility and upper gastrointestinal symptoms in patients with diabetes. AIM: To evaluate the motor, sensory and incretin responses to intraduodenal nutrients in patients with type 1 diabetes and in controls. METHODS: Eight type 1 diabetes patients (two with autonomic neuropathy) and nine controls were studied during euglycaemia. A manometric catheter was positioned across the pylorus, and nutrient was infused intraduodenally (90 kcal over 30 min). Blood glucose and plasma glucagon-like peptide 1 and gastric inhibitory polypeptide were measured, and sensations were assessed with visual analogue questionnaires. RESULTS: During nutrient infusion, neither the number of antral waves nor the stimulation of phasic or basal pyloric pressures differed between patients and controls. Upper gut sensations and areas under the plasma incretin peptide curves did not differ between the groups. CONCLUSIONS: During euglycaemia, the upper gastrointestinal motor, sensory and incretin peptide responses to small-intestinal nutrient are comparable in patients with relatively uncomplicated type 1 diabetes and in healthy subjects.

Adult↗
PubMed2004

A longitudinal study of bone-related biochemical changes at the menopause.

OBJECTIVE: To evaluate the effects of the menopause on bone-related biochemical variables in a longitudinal study. DESIGN: Recruitment by advertisement of premenopausal women over the age of 44 for measurement of selected variables and collection of blood and urine samples for deep freezing, followed by annual check of menopausal status and repeat collection of blood and urine samples for deep freezing after the menopausal transition. PATIENTS: A total of 104 women with confirmed premenopausal status and on no treatment likely to affect calcium or bone metabolism were admitted to the study over a period of 2 years. After 8 years, 43 of the volunteers had passed through the menopause and the study was closed. MEASUREMENTS: Radiocalcium absorption was measured at the first attendance and again after the menopausal transition. Calcium and other relevant variables were measured consecutively on paired thawed-out samples of blood and urine. RESULTS: The data were complete in 34 subjects. In these women, there were highly significant correlations between the first and second measurements of most variables - serum calcium and fractions, radiocalcium absorption, vitamin D metabolites, PTH and others - indicating significant 'tracking' of these variables across the menopause. Within that framework there were significant rises in serum total and calculated ionized calcium (both P < 0.001) without change in mean serum parathyroid hormone (PTH). Radiocalcium absorption fell (P < 0.001) without change in serum 1,25D. There was a rise in fasting urinary calcium (P < 0.001) which could not be explained by the rise in filtered load and therefore represented a fall in TmCa (P < 0.001). There were significant rises in urinary bone resorption markers, pyridinoline and deoxypyridinoline (P < 0.001). CONCLUSIONS: We conclude that the menopausal rise in calculated serum ionized calcium without fall in PTH, indicates a change in PTH set-point, and that the falls in gastrointestinal absorption and renal tubular reabsorption of calcium reflect the loss of an oestrogen action at these two sites. Although these changes are sufficient to explain the rise in calcium requirement at the menopause, the association of high bone resorption with normal serum PTH suggests also an increased sensitivity of bone to the action of parathyroid hormone. There is significant 'tracking' of many variables across the menopause despite very significant changes in their absolute values.

Adult↗
PubMed2004

Diet, food intake, and disturbed physiology in the pathogenesis of symptoms in functional dyspepsia.

Functional dyspepsia (FD) remains a relatively poorly characterized gastrointestinal disorder of unknown etiology that is frequently difficult to manage. A systematic review of the literature relating to food intake and FD is summarized here. Many patients with FD report symptoms after meal ingestion, including fullness, bloating, epigastric pain, nausea, and vomiting, and this has been interpreted as indicative of an underlying "motor disorder of the stomach or small intestine." Such hypotheses are, however, still largely unsubstantiated, and the data that do exist are inconclusive, particularly as few studies have directly examined the temporal relationships between dyspeptic symptoms, meal ingestion, and disordered gastric motility. Moreover, studies attempting to relate symptoms to specific disturbances in gastric motor function have, in most cases, not evaluated symptoms concurrently with the function test, and/or have used suboptimal symptom scoring to quantify symptoms. Furthermore, the term "early satiety" has been used loosely as a symptom, rather than a quantitative measure of food intake. Currently, the most widely accepted mechanism underlying FD is visceral hypersensitivity, which may contribute to both enhanced motor and symptomatic responses to food ingestion. However, the possible contribution of food and dietary habits to the induction and/or exacerbation of dyspeptic symptoms represents a relatively new area-despite frequent reports by patients that their symptoms are often related to food ingestion; this association has not been formally assessed. Dietary assessments have frequently implicated fatty foods in symptom induction, and these findings are supported by laboratory-based studies, particularly the demonstration that FD patients more often experience symptoms after intraduodenal infusions of fat, than glucose. Further studies into the potential role of dietary factors in the induction of dyspeptic symptom are required to establish whether dietary therapies have any place in the management of FD.

Diet↗
PubMed2004

Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations.

Acute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3-10.5, median or interquartile range) to 10 (9.5-14.5) per hour, P < 0.02] and volume-controlled [4 (2.5-7.5) to 10.5 (7-12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.

Adult↗
PubMed2004

Leptin prevents obesity induced by a high-fat diet after diet-induced weight loss in the marsupial S. crassicaudata.

The aims of this study were to determine in the marsupial Sminthopsis crassicaudata, the effects of leptin on food intake, body weight, tail width (a reflection of fat stores), and leptin mRNA, after caloric restriction followed by refeeding ad libitum with either a standard or high-fat preferred diet. S. crassicaudata (n = 32), were fed standard laboratory diet (LabD; 1.01 kcal/g, 20% fat) ad libitum fo 3 days. On days 4-10, animals received LabD at 75% of basal intake and then (days 11-25) were fed either LabD or a choice of LabD and mealworms (MW; 2.99 kcal/g, 30% fat); during this time, half the animals (n = 8) in each group received either leptin (2.5 mg/kg) or PBS intraperitoneally two times daily. On day 26, animals were killed and fat was removed for assay of leptin mRNA. At baseline, body weight, tail width, and food intake were similar in each group. After caloric restriction, body weight (P < 0.001) and tail width (P < 0.001) decreased. On return to ad libitum feeding in the PBS-treated animals, body weight and tail width returned to baseline in the LabD-fed animals (P < 0.001) and increased above baseline in the MW-fed animals (P < 0.001). In the LabD groups, tail width (P < 0.001) and body weight (P < 0.001) decreased after leptin compared with PBS. In the MW groups, the increase in tail width (P < 0.001) and body weight (P = 0.001) were attenuated after leptin compared with PBS. The expression of leptin mRNA in groups fed MW were greater in PBS than in leptin-treated animals (P < 0.05). Therefore, after diet-induced weight loss, leptin prevents a gain in fat mass in S. crassicaudata; this has potential implications for the therapeutic use of leptin.

Animals↗
PubMed2004

The effects of age and other variables on serum parathyroid hormone in postmenopausal women attending an osteoporosis center.

It has been known for many years that serum PTH rises with age, and it has been suggested that this rise may contribute to bone loss in postmenopausal women. It has been variously attributed to declining renal function, declining calcium absorption efficiency, and declining serum 25-hydroxyvitamin D [25(OH)D] levels. We studied the effects of age, weight, renal function, radiocalcium absorption, serum ionized calcium, and serum 25(OH)D on serum PTH levels in 918 postmenopausal women attending an osteoporosis center. On simple linear regression, serum PTH was a positive function of age (P = 0.003) and weight (P < 0.001) and an inverse function of serum 25(OH)D (P < 0.001) and serum ionized calcium (P = 0.002). On stepwise regression, serum 25(OH)D was the most significant (negative) determinant of serum PTH, followed in decreasing order of significance by serum ionized calcium (negative) and body weight and age (positive). Serum PTH was not related to radiocalcium absorption. The reciprocal relation between serum PTH and serum 25(OH)D could not be explained by the serum concentration of 1,25-dihydroxyvitamin D, which did not change with age. After adjustment for serum ionized calcium, body weight, and age, the rise in serum PTH appeared to start when serum 25(OH)D fell less than 80 nmol/liter.

Aged↗
PubMed2004

Effect of variations in small intestinal glucose delivery on plasma glucose, insulin, and incretin hormones in healthy subjects and type 2 diabetes.

The determinants of postprandial blood glycemia are controversial. We assessed the effects of variations in the initial rate of small intestinal glucose delivery on blood glucose, plasma insulin, and incretin responses in both health and type 2 diabetes. Eight controls and eight patients with type 2 diabetes managed by diet alone underwent paired studies. On both days subjects received an intraduodenal glucose infusion (t = 0-120 min); on one day the infusion rate was variable, being more rapid initially (3 kcal/min) between t = 0 and 15 min and slower (0.71 kcal/min) subsequently (t = 15-120 min), whereas on the other day, the infusion rate was constant (1 kcal/min) from t = 0 to 120 min (i.e. on both days 120 kcal of glucose were administered). Between t = 0-180 min blood glucose, plasma insulin and plasma glucose-dependent insulin-releasing polypeptide were greater with the variable, compared with the constant, infusion. Between t = 0 and 30 min the magnitude of the rise in plasma glucagon-like peptide-1 was greater with the variable, compared with the constant infusion (P < 0.01, both groups). We conclude that modest variations in the initial rate of duodenal glucose entry may have profound effects on subsequent glycemic, insulin, and incretin responses.

Biological Availability↗
PubMed2004

Therapeutic basilar artery occlusion for management of medically refractory basilar artery stenosis: case report.

OBJECTIVE AND IMPORTANCE: To describe a novel therapeutic approach (endovascular basilar artery occlusion) to a notoriously difficult-to-manage clinical condition (actively symptomatic high-grade basilar artery stenosis) on the basis of assessment of the patient-specific mechanism of disease. CLINICAL PRESENTATION: An 81-year-old woman presented with recurrent episodes of brainstem ischemia refractory to aggressive medical therapy. Cerebral angiography revealed a high-grade proximal basilar artery stenosis. On the basis of clinical presentation and angiographic findings, the pathogenesis of this complex of symptoms was thought to be embolic rather than hemodynamic. INTERVENTION: Endovascular coil occlusion of the basilar artery was used, with excellent outcome (cessation of ischemic symptoms and independent level of functioning at 1 yr). CONCLUSION: Successful endovascular management of intracranial occlusive disease requires understanding of the mechanism responsible for the patient's symptoms.

Aged↗
PubMed2004

Altered arterial homeostasis and cerebral aneurysms: a review of the literature and justification for a search of molecular biomarkers.

DESPITE THE CATASTROPHIC consequence of ruptured intracranial aneurysms, very little is understood regarding their pathogenesis, and there are no reliable predictive markers for identifying at-risk individuals. Given that intracranial aneurysms have a strong but complex genetic component and well-characterized modifiable risk factors, it seems likely that the most valuable approach to developing minimally invasive diagnostic and prognostic tools will involve a multifactorial model that includes both genetic and environmental risk factors. Unfortunately, the genetic basis of intracranial aneurysms is poorly described, and reports describing the association of nonrandom deoxyribonucleic acid sequence variation with intracranial aneurysms have been limited to a handful of ad hoc studies that have focused on a variety of markers in small populations. One reason for this lack of coordinated analysis of the genetic basis of intracranial aneurysms is that the molecular pathogenesis and pathobiological characteristics of the disease are poorly described, so candidate marker selection has been problematic. Few studies have addressed the molecular pathological basis of intracranial aneurysms or the possible mechanisms of intracranial aneurysm formation. In this regard, candidate gene selection strategies have relied almost exclusively on limited knowledge of monogenic disorders such as Ehlers-Danlos syndrome and Marfan's syndrome, in which intracranial aneurysm is a feature of a spectrum of syndromic phenotypes. Without exception, these approaches have not affected the clinical identification and/or management of intracranial aneurysms significantly. Therefore, it is imperative that coordinated large-scale efforts in genetics, molecular biology, and genetic epidemiology are implemented to overcome these obstacles and drive developments in the field. In this review, we summarize the current screening modalities for intracranial aneurysms, review the current state of understanding relating to the genetic basis of intracranial aneurysms, and suggest a broader theory of aneurysm pathogenesis to form the foundation of a coordinated molecular search for biological markers that may be associated with aneurysm formation and rupture.

Cerebral Arteries↗
PubMed2004

Altered arterial homeostasis and cerebral aneurysms: a molecular epidemiology study.

OBJECTIVE: We hypothesized that patients with intracranial cerebral aneurysms (IAs) harbor a molecular defect in the process responsible for maintaining arterial integrity (arterial homeostasis). In this study, we undertook a preliminary assessment of differential expression of key molecules involved with each phase of homeostasis: arterial flow modulation, arterial tear and repair, and the ensuing extracellular matrix. METHODS: Key molecules from each phase of the arterial homeostatic process were selected: prostacyclin-stimulating factor, implicated with arterial flow modulation; PNUT and RAI, involved with tissue repair and arterial remodeling; and Type III collagen and fibronectin, which are key constituents of the extracellular matrix. A small sample of the IA dome was harvested at the time of surgical repair from both ruptured and unruptured domes. Pericranial vascular tissue was harvested from a sample of the superficial temporal artery (STA) or occipital artery from aneurysmal and nonaneurysmal patients undergoing craniotomy for unrelated conditions. Statistical analysis examining expression of each marker was performed initially using dichotomous analysis (presence or absence of expression), followed by an assessment of quantitative differences in expression. Initial analysis was restricted to the pair consisting of dome and STA harvested from each individual patient. This was followed by a pooled analysis in which all domes and STAs were respectively pooled. RESULTS: A total of 86 tissue samples were studied, including 24 IA domes, STA samples from 43 aneurysmal patients, and STA samples from 19 nonaneurysmal patients. We found that the degree of prostacyclin-stimulating factor and RAI expression was reduced in ruptured aneurysm domes when compared with STAs from IA patients (odds ratio, 0.26; 95% confidence interval [CI], 0.08-0.89; and odds ratio, 0.18; 95% CI, 0.03-0.94, respectively). Type III collagen expression also was reduced among ruptured domes when compared with STA (P = 0.042). These differences were found to be independent of the effects of smoking with adjusted odds ratios of 0.25 (95% CI, 0.08-0.77) and 0.18 (95% CI, 0.04-0.79), respectively, for prostacyclin-stimulating factor and RAI. No statistically significant differences were noted among the unruptured domes. CONCLUSION: These preliminary data suggest an impaired ability to express proteins responsible for flow modulation and arterial repair within the ruptured domes when compared with control pericranial tissue. The study generates a hypothesis of impaired arterial homeostasis with a reduced ability to modulate hemodynamic flow with perhaps increased microinjury. This is exacerbated further by an impaired molecular ability to repair the vessel wall, culminating in aneurysm rupture. The study has limitations based on the use of pericranial tissue as the control and the relatively small sample size. Nevertheless, this study suggests that altered arterial homeostasis warrants further investigation in hopes of better understanding IA pathogenesis.

Adult↗
PubMed2004

Successful management of post-tumor resection middle cerebral artery thrombosis with stent-assisted angioplasty and thrombolytic therapy: case report.

OBJECTIVE AND IMPORTANCE: To describe successful endoluminal revascularization of an acute M1 occlusion 4 days after craniotomy and tumor resection. CLINICAL PRESENTATION: A 16-year-old right-handed girl presented with a 1-month history of daily headaches. The neurological examination was normal. Magnetic resonance imaging and computed tomography demonstrated a mass consistent with an epidermoid tumor compressing the left upper pons, left cerebral peduncle, and mesial left temporal lobe. INTERVENTION: A combination of low-dose antiplatelet agents administered intra-arterially and stent-assisted angioplasty was used. Successful endoluminal revascularization was achieved. Acute complications such as intracranial stent-thrombosis and/or intracranial hemorrhage were successfully avoided. CONCLUSION: In the acute postoperative period, most current chemical thrombolytic protocols are contraindicated because of the prohibitive risk of iatrogenic intracranial hemorrhage. With an understanding of the pharmacokinetics of the currently available antiplatelet drugs, combined chemical and mechanical thrombolysis may be used in the acute postoperative setting for endoluminal recanalization.

Adolescent↗
PubMed2004

Trigeminal neuralgia and glossopharyngeal neuralgia: two orofacial pain syndromes encountered by dentists.

BACKGROUND: Dentists frequently evaluate patients for oropharyngeal pain that may or may not eventually be related to oral pathology. Two rare neurological disorders that present with severe orofacial pain are trigeminal neuralgia, or TN, and glossopharyngeal neuralgia, or GPN. Both are secondary to cranial nerve compression by arteries and veins at the point at which the nerves exit the pons and brainstem. RESULTS: The authors present the results for two series of patients treated for TN and GPN. Significant success can be seen after intracranial microvascular decompression for both disorders, with low complication rates. Short- and long-term outcomes depend on proper patient selection. CLINICAL IMPLICATIONS: It is important for practitioners to recognize these syndromes and properly refer patients to a neurosurgeon experienced in treating such disorders. This can help the dentist and patient avoid oral procedures that will not alleviate the painful symptoms.

Anticonvulsants↗
PubMed2004

Does the response of bone mass to calcium supplements depend on calcium absorption efficiency?

OBJECTIVE: Calcium supplements can reduce bone resorption and slow bone loss after the menopause, but these effects may be limited by poor intestinal absorption. Since the increase in blood ionised calcium and decrease in serum parathyroid hormone after a calcium load are diminished in patients with poor calcium absorption, we aimed to see whether the response of bone mineral content (BMC) to calcium is related to initial calcium absorption. DESIGN: We retrospectively examined the changes in forearm BMC in 164 patients (139 women and 25 men) receiving calcium therapy alone for low bone density in a university hospital. METHODS: BMC was measured in a Molsgaard single energy absorptiometer and calcium absorption in a single blood sample 1 h after a dose of 5 microCi (45)Ca in 20 mg calcium carrier. Results were analysed by simple and multiple regression analysis. RESULTS: Mean forearm BMC did not change significantly over the mean 43 (S.D., 33) months of treatment (1.023 (0.247) to 1.017 (0.246) g/cm). The annual percentage of change was positively related to both body weight (r=0.180; P=0.020) and radiocalcium absorption (r=0.185; P=0.017). Multiple linear regression confirmed that both variables contributed to the change in BMC (P=0.023 and 0.019 respectively). The mean annual percentage of change in BMC on calcium therapy was not related to age, initial BMC, serum 1,25-dihydroxyvitamin D or fasting urinary calcium/creatinine ratio. CONCLUSIONS: These results support our earlier studies which suggest that poor calcium absorption limits the response of bone to calcium supplements.

Adult↗
PubMed2004

Meropenem administered as a prolonged infusion to treat serious gram-negative central nervous system infections.

The treatment of gram-negative infection of the central nervous system (CNS) presents a clinical challenge due to antibiotic resistance and difficulties with penetration into the cerebrospinal fluid (CSF). Two patients with gram-negative CNS infections were treated successfully with high-dose, prolonged infusions of meropenem. The CSF meropenem concentrations exceeded the minimum inhibitory concentration of the pathogen for virtually the entire dosing interval in both cases. Our experience demonstrates that dosage modification to maximize pharmacodynamic targets and bactericidal activity may be practically applied to optimize antibiotic treatment for difficult-to-treat CNS infections.

Adult↗
PubMed2004

Effects of Tisseel fibrin glue on the central nervous system of nonhuman primates.

For many years, neurosurgeons and otolaryngologic surgeons have used the fibrin glue product Tisseel to repair skull-base spinal fluid leaks and to help secure repairs following anterior cranial-base surgery. Despite the widespread use, the potential focal cerebral toxicity of this fibrin glue has never been investigated. We studied the safety of Tisseel applied directly to neural tissue (brain parenchyma, cervical cord, and C3-C6 spinal roots) of 6 monkeys (Macaca nemestrina) to determine if any underlying biochemical injury would occur. Another 3 animals that served as controls received saline rather than Tisseel. We found that median nerve electroencephalographic tracings and somatosensory evoked potentials in the experimental and control animals were identical. Likewise, cerebrospinal fluid indicators of neuronal or brain injury, inflammatory responses, and infection were negative in both groups. Finally, there were no significant differences between the two groups with respect to edema volumes and apparent diffusion coefficient values. We conclude that Tisseel does not induce an apparent inflammatory response or abnormal neurophysiologic or histologic response within 5 days of its application when it is applied directly to the brain parenchyma or onto the cervical spinal cord.

Animal Experimentation↗
PubMed2003

Radiocalcium absorption is reduced in postmenopausal women with vertebral and most types of peripheral fractures.

Intestinal calcium absorption accounts for 60% of the variance in calcium balance and is therefore a potentially very important determinant of bone status. Whether measured by the balance technique or with radiocalcium, it is known to be significantly reduced in postmenopausal women with vertebral and hip fractures. By contrast, there is very little information about calcium absorption in other types of postmenopausal fracture. We now report a series of 549 untreated, Caucasian postmenopausal women in whom we recorded prevalent fractures, measured radiocalcium absorption, and obtained radiographs of the lateral thoracic and lumbar spine. Of these women, 172 had no prevalent fractures, showed normal spine radiographs, and served as controls; 72 had one or more peripheral fractures but normal spine radiographs; 147 had one or more wedged or crushed vertebrae but no peripheral fractures; and 158 had a history of peripheral fracture and one or more fractured vertebrae. Age-adjusted radiocalcium absorption was significantly lower in the two groups with spinal fractures than in the controls ( P<0.001) but not in the group with peripheral fractures only. It was also lower in the cases with more than two spinal fractures than in those with two or less (P<0.001). In respect of peripheral fractures, the greatest age-adjusted absorption deficit was found in fractures of the humerus (35%) followed by hip (32%), spine (21%), wrist (19%), and rib 17% (all significant but not significantly different from each other). Lesser deficits in tibia, ankle and foot fractures were not significant but type 2 errors could not be excluded. We conclude that impaired calcium absorption is particularly associated with those fractures for which osteoporosis is a significant risk factor.

Absorption↗
PubMed2003

Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans.

The presence of nutrients in the small intestine slows gastric emptying and suppresses appetite and food intake; these effects are partly mediated by the release of gut hormones, including CCK. We investigated the hypothesis that the modulation of antropyloroduodenal motility, suppression of appetite, and stimulation of CCK and glucagon-like peptide-1 secretion by intraduodenal fat are dependent on triglyceride hydrolysis by lipase. Sixteen healthy, young, lean men were studied twice in double-blind, randomized, crossover fashion. Ratings for appetite-related sensations, antropyloroduodenal motility, and plasma CCK and glucagon-like peptide-1 concentrations were measured during a 120-min duodenal infusion of a triglyceride emulsion (2.8 kcal/min) on one day with, on the other day without, 120 mg tetrahydrolipstatin, a potent lipase inhibitor. Immediately after the duodenal fat infusion, food intake at a buffet lunch was quantified. Lipase inhibition with tetrahydrolipstatin was associated with reductions in tonic and phasic pyloric pressures, increased numbers of isolated antral and duodenal pressure waves, and stimulation of antropyloroduodenal pressure-wave sequences (all P < 0.05). Scores for prospective consumption and food intake at lunch were greater, and nausea scores were slightly less, and the rises in plasma CCK and glucagon-like peptide-1 were abolished (all P < 0.05). In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodenal motility, appetite, and CCK and glucagon-like peptide-1 secretion.

Adult↗